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Author: Dr. Hassan Gargoum

Clinical Professor of Medicine, University of Saskatchewan Consultant, Cardiovascular Diseases

New guidelines for stable coronary artery disease

Written by Dr. Hassan Gargoum on . Posted in Cardiology News. No Comments on New guidelines for stable coronary artery disease

Lifestyle changes and medical therapy should be the mainstay for most patients with stable coronary artery disease, according to the new ACC/AHA/ACP guidelines for this patient group, published online November 19, 2012 in the Annals of Internal Medicine. The primary focus of interventions in these patients, according to the new guidance, should be reducing the risk of premature cardiovascular death and nonfatal MI while maintaining activity levels and a quality of life.  Patient education regarding various therapeutic options, appropriate levels of exercise, diet and weight control, and the importance of various clinical manifestations play a key role in achieving the treatment goal.

The guidelines include 48 specific recommendations relevant for primary-care physicians and emphasize patient education, managing cardiovascular risk factors, the use of medical therapy to prevent myocardial infarction and death and to relieve angina symptoms, the use of revascularization to improve survival and symptoms, and patient follow-up.

The initial approach to patient management focuses on eliminating all unhealthy behaviors, such as smoking, and promoting weight loss, physical activity, and a heart-healthy diet. Most important, the new guidelines provide an algorithm that emphasizes an evidence-based set of pharmacologic interventions intended to reduce the risk of future events. Drug therapy includes the use of antiplatelet agents, lipid-lowering drugs, particularly statins, and beta blockers. ACE inhibitors are recommended for many patients with stable coronary artery disease, such as those with diabetes or left ventricular dysfunction.

The new guidelines strongly support the importance of medical therapy as the first-line treatment for patients with stable coronary artery disease. The management begins with lifestyle intervention and eliminating unhealthy behaviors, followed by secondary prevention and pharmacotherapy.  Beta blockers are recommended as the initial treatment for relief of symptoms in patients with stable coronary artery disease, and calcium-channel blockers or long-acting nitrates are recommended when beta blockers are contraindicated or cause unacceptable side effects or when initial treatment is unsuccessful. Sublingual nitroglycerin is recommended for the immediate relief of angina. Should symptoms persist after medical therapy, physicians are advised to consider coronary artery revascularization.

For revascularization to improve symptoms, coronary artery bypass grafting (CABG) surgery or percutaneous coronary intervention (PCI) is recommended in patients with one or more significant (>70% stenosis) lesions. CABG surgery or PCI is not recommended in patients who do not meet the anatomic (>50% stenosis of the left main artery or >70% non-left main stenosis) or physiologic criteria for revascularization. In addition, PCI should not be performed if the patient is unable or unlikely to comply with dual antiplatelet therapy.

In addition, the guidelines recommend CABG or PCI to improve survival in several clinical scenarios, such as in patients with stenosis of the left main coronary artery, patients with lesions in three major coronary arteries, or patients with presumed ischemia-mediated ventricular tachycardia caused by a stenosis in a major coronary artery. PCI or CABG surgery is not recommended to improve survival in patients with stable coronary artery disease with one or more coronary lesions that are not anatomically or functionally significant.

Source:

Qaseen A, Fihn SD, Dallas P, et al. Management of patients with stable ischemic heart disease: Executive summary of a clinical practice guideline from the American College of Physicians, American College of Cardiology Foundation/American Heart Association/American Association for Thoracic Surgery/Preventive Cardiovascular Nurses Association/Society of Thoracic Surgeons. Ann Intern Med 2012

 

Noncompaction Cardiomyopathy (NCCM)

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 Isolated non-compaction cardiomyopathy (INCCM) and its typical echocardiographic appearance were first described in 1984 by Engberding and Bender.  INCCM is a heart-muscle disorder that is still little known among physicians.  In a study of children with primary cardiomyopathy of all types, NCCM was present in 9.2%. It was thus the third most common type of primary cardiomyopathy, after dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy.

Noncompaction of the ventricular myocardium is a cardiomyopathy thought to be caused by arrest of normal embryogenesis of the endocardium and myocardium. This abnormality is often associated with other congenital cardiac defects, but it is also seen in the absence of other cardiac anomalies.  Clinical manifestations are highly variable, ranging from no symptoms to disabling congestive heart failure, arrhythmias, and systemic thromboembolism. Echocardiography has been the diagnostic procedure of choice, but the correct diagnosis is often missed or delayed because of lack of knowledge about this uncommon disease and its similarity to other diseases of the myocardium and endocardium.

 Embryology and Development:

During early embryonic development, the myocardium is a loose network of interwoven fibers separated by deep recesses that link the myocardium with the left ventricular cavity. Gradual “compaction” of this spongy meshwork of fibers and intertrabecular recesses, or “sinusoids,” occurs between weeks 5 and 8 of embryonic life, proceeding from the epicardial to endocardium and from the base of the heart to the apex. The coronary circulation develops concurrently during this process, and the intertrabecular recesses are reduced to capillaries.

The normal process of trabeculation appears to involve secretion of neuregulin growth factors from the endocardium and may also involve angiogenesis factors, such as vascular endothelial growth factor and angiopoietin.

Noncompaction of the ventricular myocardium (NVM) is an uncommon finding. It is thought to be caused by arrest of the normal process of endomyocardial morphogenesis.

NCCM was first described in association with other congenital anomalies, such as obstruction of the right or left ventricular outflow tracts, complex cyanotic congenital heart disease, and coronary artery anomalies. The abnormal compaction process in these cases is not fully understood, but pressure overload or myocardial ischemia preventing regression of the embryonic myocardial sinusoids has been suggested. This process results in the persistence of deep intertrabecular recesses in communication with both the ventricular cavity and the coronary circulation.

Isolated non-compaction cardiomyopathy (INCCM) and its typical echocardiographic appearance were first described in 1984 by Engberding and Bender is characterized by persistent embryonic myocardial morphology found in the absence of other cardiac anomalies to explain the abnormal development. In such cases, the resultant deep recesses communicate only with the ventricular cavity, not the coronary circulation.

The left ventricle is uniformly affected, but biventricular noncompaction has been reported, with right ventricular noncompaction described in less than one-half of patients. Because of difficulty in distinguishing normal variants in the highly trabeculated right ventricle from the pathological noncompacted ventricle, several authors dispute the existence of right ventricular noncompaction.

Both familial and sporadic forms of noncompaction have been described.

In the original report of INCCM, which predominantly involved children, familial recurrence was seen in half of patients.  Familial recurrence was seen in 18% in the largest reported adult population with INCCM, although the authors reported that incomplete screening of siblings may account for the lower percentage compared with the earlier report.

 Epidemiology:

The prevalence of this disease in adults remains unclear. In observational studies, NCCM has been found in 0.014% to 0.26% of all adults referred to an echocardiography laboratory. The incidence of NCCM in the general population has been estimated at 0.05% to 0.25% per year. The diagnosis is presumably often missed, because the disease is still not as well-known as it should be among physicians at large.

Clinical Features and Pathophysiology:

Three major clinical manifestations of noncompaction have been described, including: Heart failure, arrhythmias, and embolic events.

Findings vary among patients, ranging from asymptomatic left ventricular dysfunction to severe, disabling congestive heart failure.

Over two thirds of the patients in the largest series with NCCM had symptomatic heart failure.

Coronary angiography reveals no abnormalities in patients with NCCM, but positron emission tomography (PET) shows a diminished reserve of coronary blood flow in the compact and non-compact myocardial segments of the left ventricle, presumably because of impaired microcirculation. Similar findings are obtained with single photon emission computerized tomography (SPECT).

Depressed ventricular systolic function has been noted in 63% of patients.  Both systolic and diastolic ventricular dysfunction has been described.

Restrictive hemodynamics by cardiac catheterization, as well as an initial presentation of NCCM as a restrictive cardiomyopathy, have been described in children with NCCM.

Left ventricular dysfunction developed in the vast majority, regardless of the presence or absence of symptoms at initial diagnosis.

Furthermore, marked trabeculation can impair the diastolic function of the left ventricle as well, with abnormal relaxation and restricted filling.

The origin of systolic dysfunction in noncompaction is unclear, but it has been suggested that subendocardial hypoperfusion and microcirculatory dysfunction playing roles in ventricular dysfunction and arrhythmogenesis.

These systolic and diastolic disturbances of left ventricular function, if severe enough, can lead to the clinical manifestations of heart failure that are seen in many patients with NCCM.

Arrhythmias are common in patients with ventricular noncompaction. Atrial fibrillation has been reported in over 25% of adults with NCCM. Ventricular tachyarrhythmia has been reported in as many as 47%.   Sudden cardiac death accounted for half of the deaths in the larger series of patients with NCCM.  Paroxysmal supraventricular tachycardia and complete heart block have also been reported in patients with NCCM.

Abnormalities of the resting ECG are found in the majority of patients with NCCM but findings are nonspecific and include left ventricular hypertrophy, repolarization changes, inverted T waves, ST segment changes, axis shifts, intraventricular conduction abnormalities, and AV block. Left bundle branch block has been described in 44% of adult patients with NCCM, but the reported incidence in children was much lower.

Electrocardiographic findings of the Wolff-Parkinson-White syndrome have been described in up to 15% of pediatric patients.

The occurrence of thromboembolic events, including cerebrovascular accidents, transient ischemic attacks, pulmonary embolism, and mesenteric infarction, ranged from 21% to 38%.

Embolic complications may be related to development of thrombi in the extensively trabeculated ventricle, depressed systolic function, or the development of atrial fibrillation.  Of interest, no systemic embolic events were reported in the largest pediatric series with NCCM.

An association between NCCM and facial dysmorphisms, including a prominent forehead, low-set ears, strabismus, high-arching palate, and micrognathia, has been described.

Diagnosis:

Echocardiography is the diagnostic test of choice for NCCM.  Multiple prominent ventricular trabeculations with deep intertrabecular recesses are seen. Color Doppler imaging demonstrates blood flow through these deep recesses in continuity with the ventricular cavity.

The left ventricular apical and inferior wall segments were involved in all patients in an adult population with NCCM studied by echocardiography. The right ventricular apex was involved in 41%.

Depressed left ventricular systolic function was the rule, with a mean calculated ejection fraction of 33% in 28 patients examined. Impairment of diastolic function as assessed by mitral inflow and pulmonary venous flow Doppler was observed in all, including a restrictive filling pattern in 36%.

Prominent trabeculations (although virtually always < 3 in number in normal variants), apical hypertrophic cardiomyopathy, dilated cardiomyopathy, arrhythmogenic right ventricular dysplasia, endocardial fibroelastosis, cardiac metastases, and left ventricular thrombus are important differential diagnostic considerations. Transesophageal echocardiography may be used when transthoracic studies cannot reliably exclude other processes. One report described the use of contrast echocardiography with sonicated albumin in a patient with NCCM. Contrast echocardiography may be helpful when standard echocardiographic image quality is limited or the diagnosis is questionable.

Cardiac magnetic resonance imaging (MRI) is a further method that can be used to diagnose NCCM accurately. Cardiac magnetic resonance imaging has become the method of choice to confirm or rule out left ventricular noncompaction, because echocardiography cannot allow proper visualisation of the apex in some cases.

MRI provides good correlation with echo for localization and extent of noncompaction and is useful in cases with poor echocardiographic image quality.

In addition, the demonstration of differences in MRI signal intensity in noncompacted myocardium may help identify substrate for potentially lethal arrhythmias.

Management:

Treatment for noncompaction of the ventricular myocardium focuses on the 3 major clinical manifestations:  Heart failure, arrhythmias, and systemic embolic events. Standard medical therapy for systolic and diastolic ventricular dysfunction is warranted. Cardiac transplantation has been used for those with refractory congestive heart failure.

The beneficial effects of the beta blocker carvedilol on left ventricular function, mass, and neurohormonal dysfunction in an infant with NCCM have been described.  Because of the frequency of ventricular tachycardia and significant risk of sudden cardiac death and systemic embolism, assessment for atrial and ventricular arrhythmias by ambulatory ECG monitoring should be performed annually. As more information is gathered about NCCM and risk of sudden cardiac death, implantable defibrillator technology may have an expanded role.                                                                                                                                                                                                                                                                                                            Biventricular pacemakers may have a role in the treatment of NCCM patients with heart failure, reduced left ventricular function, and prolonged intraventricular conduction.

Prevention of embolic complications is also an important management issue, and several authors have recommended long-term prophylactic anticoagulation for all patients with ventricular noncompaction whether or not thrombus has been found. Because of the familial association described with noncompaction, screening echocardiography of first degree relatives is recommended. Given the high percentage of associated neuromuscular disorders reported in patients with NCCM, neurological and musculoskeletal evaluations are also recommended.

Prognosis:

Although the prognosis for patients with NCCM varies, nearly 60% of patients described in one large series had either died or undergone cardiac transplantation within 6 years of diagnosis.

Two of 8 in the initially asymptomatic group of this series died during the follow-up period, both having documented sustained ventricular tachycardia and one with sudden cardiac death. Similarly, in a series of 34 adults with NCCM, 47% either died or underwent cardiac transplantation during the follow-up period of 44 months.

The occurrences of systemic emboli, ventricular arrhythmias, and death were considerably lower in the largest pediatric series with NCCM when compared with adults and the initial case series by Chin et al, although nearly 90% of patients followed for up to 10 years developed left ventricular dysfunction.

Oechslin et al reported that certain clinical characteristics were observed significantly more frequently in nonsurvivors compared with survivors with NCCM, including:

1)   –  Higher left ventricular end diastolic diameter on presentation.

2)   –  New York Heart Association class III-IV.

3)   –  Permanent or persistent atrial fibrillation.

4)   –  Bundle branch block.

Patients with these high risk features are candidates for early, aggressive interventions, including consideration of cardioverter-defibrillator implantation and evaluation for transplantation.

Conclusion:

Non-compacted cardiomyopathy is a congenital malformation that can occur as an isolated entity or associated with other pathologies of the heart and can often involve both ventricles. A ratio of noncompacted: compacted wall greater than 3 and involvement of three or more segments are signs of poor prognosis associated with greater clinical deterioration (functional class III/IV) and ventricular arrhythmias.

A high index of suspicion for non-compaction is necessary as the condition may lead to serious heart failure, thromboembolic events, ventricular tachyarrhythmia or death. Early recognition of non-compaction may give better follow-up and management of patients with this condition.

The clinical picture does not provide sufficiently specific evidence to establish the diagnosis. Echocardiography is the diagnostic cornerstone. Treatment should be directed towards prevention and management of heart failure, ventricular arrhythmias and prevention of thromboembolic events. The long-term prognosis of non-compaction cardiomyopathy is poor.

Unresolved issues:

  • Definitive      echocardiographic and CMR criteria for diagnosis.
  • Prevalence of RV      involvement and diagnostic criteria.
  • Whether prognosis      can be improved by early diagnosis-treatment.
  • Comprehension of      the poor genotype-phenotype correlation.

Suggested Readings:

1)   – Weiford B.C., et al; Noncompaction of the Ventricular Myocardium. Circulation 2004, 109:2965-2971.

2)   – Engberding R, et al. Isolated Non-compaction Isolated Cardiomyopathy. Dtsch Arztebl Int. 2010 March; 107(12): 206–213.

3)   – Patil VC, Patil HV. Isolated Non-compaction Cardiomyopathy presented with Ventricular Tachycardia. Hear Views, 2011 Apr-Jun; 12(2):74-78

 

 

 

 

European Society of Cardiology (ESC) Guidelines on the management of valvular heart disease (version 2012)

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 A great number of guidelines have been issued in recent years by the European Society of Cardiology (ESC) as well as by other societies and organizations. Because of their impact on clinical practice, quality criteria for the development of guidelines have been established, in order to make all decisions transparent to the user.

The first step of evaluation of patients with valvular heart disease begins by obtaining a good clinical history. The aim of obtaining a case history is to assess symptoms and to evaluate for associated comorbidity. Essential questions in the evaluation of a patient for valvular intervention should include the following:

• Is valvular heart disease severe?

• Does the patient have symptoms?

• Are symptoms related to valvular disease?

• What are patient life expectancy and expected quality of life?

• Do the expected benefits of intervention (vs. spontaneous outcome) outweigh its risks?

• What are the patient’s wishes?

• Are local resources optimal for planned intervention?

The following are 10 points to remember about these new ESC guidelines on the management of valvular heart disease (VHD):

1. Echocardiography is the key technique used to confirm the diagnosis of VHD, as well as to assess its severity and prognosis. It is indicated in any patient with a murmur, unless no suspicion of valve disease is raised after the clinical evaluation. Transesophageal echocardiography should be considered when transthoracic echocardiography is of suboptimal quality or when thrombosis, prosthetic dysfunction, or endocarditis is suspected.

2. Exercise Stress Testing: The primary purpose of exercise testing is to unmask the objective occurrence of symptoms in patients who claim to be asymptomatic or have doubtful symptoms. Exercise testing has an additional value for risk stratification in AS. Exercise testing will also determine the level of authorized physical activity, including participation in sports.        The use of stress tests to detect coronary artery disease (CAD) associated with severe VHD is discouraged because of their low diagnostic value and potential risks.

Exercise echocardiography may provide additional information in order to better identify the cardiac origin of dyspnea—which is a rather unspecific symptom—by showing, for example, an increase in the degree of mitral regurgitation/aortic gradient and in systolic pulmonary pressures.

3. Coronary angiography is recommended before valve surgery in patients with severe VHD and any of the following: history of CAD; suspected myocardial ischemia; left ventricular (LV) systolic dysfunction; in men aged over 40 years and postmenopausal women; and ≥1 cardiovascular risk factor.

Coronary angiography can be omitted in young patients with no atherosclerotic risk factors (men <40 years and premenopausal women) and in rare circumstances when its risk outweighs benefit, e.g. in acute aortic dissection, a large aortic vegetation in front of the coronary ostia, or occlusive prosthetic thrombosis leading to an unstable hemodynamic condition.

4. In severe aortic regurgitation, surgery is indicated in symptomatic patients, in asymptomatic patients with resting LV ejection fraction (LVEF) ≤50%, and in patients undergoing coronary artery bypass grafting (CABG) or surgery of ascending aorta, or on another valve.

5. Aortic valve replacement is indicated in patients with severe aortic stenosis (AS) and any symptoms related to AS, in patients with severe AS undergoing CABG, surgery of the ascending aorta or another valve, in asymptomatic patients with severe AS and systolic LV dysfunction (LVEF <50%) not due to another cause, and in patients with severe AS and abnormal exercise test showing symptoms on exercise clearly related to AS.

6. Transcatheter aortic valve implantation (TAVI) should only be undertaken with a multidisciplinary ‘heart team’ including cardiologists and cardiac surgeons and other specialists if necessary, and should only be performed in hospitals with cardiac surgery on-site.

7. TAVI is indicated in patients with severe symptomatic AS who are not suitable for AVR as assessed by a ‘heart team,’ and who are likely to gain improvement in their quality of life, and to have a life expectancy of more than 1 year after consideration of their comorbidities.

8. In severe primary mitral regurgitation, mitral valve repair should be the preferred technique when it is expected to be durable. Surgery is indicated in symptomatic mitral regurgitation patients with LVEF >30% and LV end-systolic dimension (LVESD) <55 mm and in asymptomatic patients with LV dysfunction (LVESD ≥45 mm and/or LVEF ≤60%).

9. Percutaneous mitral commissurotomy is indicated in symptomatic mitral stenosis patients with favorable characteristics, and in symptomatic patients with contraindication or high risk for surgery.

10. For valve replacement, a mechanical prosthesis is recommended according to the desire of the informed patient and if there are no contraindications for long-term anticoagulation, and a bioprosthesis is recommended when good quality anticoagulation is unlikely (compliance problems; not readily available) or contraindicated because of high bleeding risk (e.g., prior major bleed, comorbidities, unwillingness, compliance problems, lifestyle, occupation).

Source: 1)- Vahnnian A, et al. Eur heart J 2012; 33:2451-2496; 2)- Mukherjee D.: Cardiosource.

 

Valve Prosthesis–Patient Mismatch

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The concept/phenomenon of valve prosthesis/patient mismatch (VP–PM) was first described in 1978.  All prosthetic heart valves have some degree of VP–PM.

The original paper (in 1978) that described valve prosthesis–patient mismatch (VP–PM) stated that “Mismatch can be considered to be present when the effective prosthetic heart valve area, after insertion into the patient, is less than that of a normal human valve”. It must be noted that all prosthetic heart valves (PHVs) are smaller than normal and thus are inherently stenotic.  The PHV mismatch was stated to be “usually mild to moderate in severity and often of no immediate clinical significance.” However, severe mismatch may lead to significant symptomatic and hemodynamic deterioration and increased mortality.

With the publication of VP–PM, surgeons were more careful and inserted the largest PHV that could be safely inserted. PHVs with improved hemodynamic profile have also been developed. As a result severe VP–PM has become a much less common clinical problem. The overwhelming majority of a large number of scientific publications have related to the aortic valve and not to mitral valve VP–PM.

How should VP–PM be measured?

Different parameters have been evaluated to assess for the severity of VP–PM. The most commonly used measures of valve size is the EOAi.

The EOA is a physiological parameter analogous to the native AVA. The EOA can be measured both invasively and noninvasively using echocardiography/Doppler or magnetic resonance imaging. The most readily and widely available method is echocardiography/Doppler. The accuracy of EOA echocardiographic measurement in the bioprosthetic valve is limited by the same pitfalls that are present in the measurement of the AVA; in particular, the LV outflow tract diameter may be more difficult to measure because of reverberation artifact caused by the prosthetic heart valve, but in these instances, the sewing ring diameter may be a sufficient surrogate. In the bileaflet mechanical valve, the central orifice may produce a high-velocity jet, causing an underestimation of the EOA. Pressure recovery occurs with both bioprosthetic and mechanical heart valves, although the implications of pressure recovery in PHVs have not yet been clarified. The EOAi has a complex relationship with the mean gradient across the aortic valve and PHV.

Assessment of severity of VP–PM

With aortic VP–PM the obstruction to the LV outflow tract is similar to that seen with native AS. Thus, the severity of aortic VP–PM should be assessed by the same criteria as for severe AS. Severe aortic stenosis is defined as mean aortic valve gradient, measured after energy recovery (also called pressure recovery), of ≥50 mm Hg and an AVA index of ≤ 0.6 cm²/m². ); it would be reasonable that this criterion should also be applied to severe VP–PM.

 

 

Grading

AVA and EOA, cm2

AVA Index and EOAi, cm2/m2
Mild

>1.5

>0.9
Moderate

>1.0–1.5

>0.6–0.9
Severe

≤1.0

≤0.6
Very severe/critical

≤0.7

≤0.4

 

When should the severity of VP–PM be determined?

4 phases of physiological healing of mechanical and bioprosthetic PHVs have been described; they are “platelet and fibrin deposition, inflammation, granulation tissue, and finally encapsulation. Long-term device fibrous encapsulation with extension to adjacent tissues adds to structural stability.” Bioprosthetic valves undergo morphological changes of both the tissue material as well as the supporting structures, which may contribute to VP–PM. Valve leaflets become covered by fibrin, platelets, and other cellular material. The matrix of the leaflets undergoes microcalcification as well insulation with plasma materials, causing changes in the matrix structure. These changes may change the resistive properties of leaflet materials. In both mechanical and bioprosthetic valves, a fibrous sheath may also encapsulate the supporting structure of the valve, encroaching on the PHV orifice and also possibly causing valve leaflet or disk immobilization.

For PHVs of the same size, there was a wide range of EOAs. Two echocardiographic/Doppler studies from the Mayo Clinic of patients studied within 1 week of mitral porcine mitral bioprosthesis and of tricuspid mechanical prostheses showed a wide range of gradients and EOAs with the same size of PHV, even in the same brand of PHV.

There are at least several explanations for these findings. 1) PHVs of the same labeled size are not necessarily of precisely the same size. Bioprostheses and other biological valves may also have differences in tissue materials. 2) There are variations from patient to patient with regard to healing changes, hemodynamic conditions, and pressure recovery.

It is best to measure VP–PM early (at 1 week after PHV implantation or at time of hospital discharge) to determine the variations in actual size of the PHV that was implanted in an individual patient. Importantly, VP–PM should also be assessed at 6 to 12 months when the physiological and other morphological changes in the PHV are mostly complete. The severity of VP–PM determined at this time can be expected to determine the long-term impact of VP–PM on patients’ outcomes.

Conclusions:

It must be noted that all prosthetic heart valves (PHVs) are smaller than normal and thus are inherently stenotic.

1) – EOAi should be measured at 1 to 4 weeks or at hospital discharge to evaluate the actual valve size that was implanted. This should also be done at 6 to 12 months to evaluate the severity of VP–PM that will affect long-term outcomes.

2) – The grading of severity of VP–PM should be similar to another common LV outflow tract obstruction, namely, valvular AS. VP–PM can be mild (EOAi >0.9 cm2/m2), moderate (EOAi >0.6 to 0.9 cm2/m2), or severe (EOAi ≤0.6 cm2/m2).

3) – Mild VP–PM, like mild AS, is unlikely to have clinically significant untoward effects. Outcomes with moderate and severe VP–PM should be evaluated separately. Moderate VP–PM is unlikely to reduce survival unless there is progression of valve obstruction, for example, with pannus formation. Severe VP–PM has negative effects on outcomes, but its effect on mortality is still unproven.

4) – Prediction of severity of VP–PM is problematic. The primary goal should be not to prevent VP–PM but rather to prevent severe VP–PM.

5) – Use of the EOAi as a continuous variable may help to define the level of severe VP–PM that results in increased mortality, and this may occur at a critical level of obstruction (≤0.4 cm2/m2).

 

References:
1)- Rahimtoola S, The problem of valve prosthesis-patient mismatch, Circulation 1978; 58:20-24.                                                                                                                                                                                                                                                                                                                  2)- Daneshuar S.A.; Rahimtoola S.H. Valve Prosthesis-Patient Mismatch (VP-PM): Long-Term Prespective. J AM Coll Cardiol 2012;60(13):1123-1135.

HRT cuts down cardiovascular risk by 50%

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A new randomized Danish study, published online October 9, 2012 in BMJ, showed that hormone-replacement therapy (HRT) in postmenopausal women, with a mean age of 50, significantly reduced the risk of the combined end point of mortality, myocardial infarction, or heart failure.

Healthy 1006 women aged 45 to 58 who were recently postmenopausal or had perimenopausal symptoms were randomized to receive HRT (n=502) or no treatment (n=504).

The participants of this study, who used HRT for more than 10 years, had a 52% reduction in cardiovascular endpoints without significant increase in risk of breast cancer or stroke.

This is considered the longest randomized trial with hard end points. The participants were also followed for a further 6 years after discontinuation of randomized treatment.

In 2002, the Women’s Health Study Initiative (WHI) showed no cardiovascular benefit from HRT and, even an indication that HRT may be harmful. However, subsequent analysis of WHI and data from other studies has suggested that the time at which HRT is first started is the key.  The women in the Danish study were 13 years younger, on average, than women in WHI (mean age 63 years). Therefore, it is important to initiate the treatment at menopause and not many years later.

 

 

55-year old male with chest pain.

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The following ECG was taken from a  55-year old male who presented to the ER with 2-hour history of persistent heavy discomfort across the anterior chest with radiation to the neck.

Risk factors: Positive family history (father had MI at age 52); hypertension; dyslipidemia.

Medications: Nifedipine XL 30 mg daily and atorvastatin 10 mg daily.

Physical examination: Heart rate 100 beats per minute, BP 130/85 mmHg,  respiratory rate 22/minute. Jugular veinous pressure is 4 cm above the sternal angle at 45 degrees. Soft S1 and S2 and prominent S4. No murmurs.

Questions:

1)- What is the ECG diagnosis?

a. Acute pericarditis.

b. Acute anterior ST elevation myocardial infarction.

c. Acute infero-posterior-lateral ST elevation myocardial infarction.

d. Acute infero-posterior-lateral with right ventricular myocardial infarction.

What is new about premature atrial contractions?

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Premature atrial contractions (PACs) occur in the majority of people aged over 50, and their frequency is independently associated with a number of risk factors.   PACs are very common and we normally say they are benign and tell the patient not to worry about them. This message should not change.  It has been known that frequent PACs increase risk of atrial fibrillation (AF) and stroke. PACs play an important role of atrial electrical activity in atrial fibrillation initiation and maintenance.

Conen et al performed a cross-sectional analysis among participants of the population-based Swiss cohort study to assess PAC prevalence and frequency. 24-hour Holter electrocardiograms were performed in a random sample of 1742 participants aged 50 years and older.

They found that 99% of people over the age of 50 had at least one PAC on 24-hour Holter monitoring.

Not surprisingly, age was one of the strongest risk factors. PAC frequency was significantly associated with age and with history of prior cardiovascular disease.

There was also a significant association between increased frequency of PACs and height. It has been known that taller people have a higher risk of atrial fibrillation; no one knows why but probably because they have a taller atrium.

Of note, hypertension and body-mass index were not significantly related to PAC frequency. This was surprising, because high blood pressure and obesity are two of the strongest risk factors for atrial fibrillation occurrence. The authors speculated that these two risk factors (high blood pressure and obesity) are exerting their effects via morphological means, but they don’t have a lot of influence on the electrical part of atrial fibrillation.

Physical activity—two hours or more per day and HDL cholesterol were inversely associated with PAC frequency.

The authors could not determine a threshold of PACs above which risk of AF is greater, but they speculated that those having more than 100 PACs in a 24-hour period would be at greater risk to develop atrial fibrillation than those having one to two per day.

While this study may not have immediate clinical implications, these findings may suggest differential risk factors for structural and electrical remodeling in the pathogenesis of atrial fibrillation.

Source: Conen D, Adam M, Roche F, et al. Premature atrial contractions in the general population: Frequency and risk factors. Circulation 2012.

Wolff-Parkinson-White Syndrome

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The heart has 4 chambers that pump blood. The 2 upper chambers are the right and left atria, and the 2 lower chambers are the right and left ventricles. The heart also has an electric system that directs the coordinated beating of these 4 chambers.

A schematic drawing of the normal heart structure and electric system (red arrows) is shown in Figure 1. A normal electric impulse originates in an area of the upper right atrium called the sinus (SA) node, and an ordinary electric activity of the heart is referred to as normal sinus rhythm. In normal sinus rhythm, an electric impulse is generated by the SA node, and that electricity spreads through the right and left atria, directing these chambers to beat.

On an electrocardiogram (ECG; bottom of Figure 1), the electric activity from the atria is seen as a small rounded deflection called a P wave. The same electric impulse then passes through a small area of tissue between the atria and ventricles called the atrioventricular (AV) node and then down through the ventricles. On the ECG, the electric activity from the ventricles results in a larger deflection called the R wave or QRS complex. Because the AV node is small, there is not enough electric activity to cause a deflection in the ECG. Therefore, the time spent by the electric impulse traveling through the AV node is represented on the ECG by a flat interval called the PR interval. In a normal heart, the AV node is a gatekeeper of sorts in that it is the only pathway for electricity that communicates from the upper chambers (atria) to the lower chambers (ventricles). The combination of electric impulses from the SA node to the atria, then through the AV node, and down to the ventricles results in 1 heartbeat. In summary, the electric activity on the ECG starts with a small deflection that results from atrial electric activity (the P wave), followed by a flat section resulting from electric activity through the AV node (the PR interval), followed by a larger deflection that results from electric activity from the ventricles (the R wave or QRS complex).

 

What Is an Accessory Pathway or Bypass Tract?

Some people are born with an extra piece of heart muscle tissue that connects directly between the atria and the ventricles, bypassing the AV node altogether. This abnormal piece of muscle is referred to as a bypass tract or an accessory pathway (Figure 2).

This extra piece of tissue can serve as a passageway for the electric signals between the atria and ventricles and allow electric activity in the ventricles to occur immediately after electric activity in the atria without having to wait for the electric impulse to travel through the AV node. In this situation, the ECG may not have much of a flat PR interval but instead may have the P wave (from atrial activity) right up against the R wave (from ventricular activity), with the R wave beginning with an upslope referred to as a delta wave (Figure 2). This delta wave results from electric activity traveling over the accessory pathway and bypassing the AV node.

Some people with an accessory pathway have a normal ECG at baseline because the accessory pathway is electrically active only when there is a fast, racing heartbeat (tachycardia) described below. Therefore, some people with accessory pathways can have completely normal ECGs like the one seen in Figure 1. This is referred to as a concealed accessory pathway.

 

How Does an Accessory Pathway Cause a Fast Heartbeat (Tachycardia)?

Not all patients with accessory pathways have fast heartbeats. Some people with a delta wave on their ECG caused by an accessory pathway will never have a problem with a fast heartbeat. In others, a rapid heartbeat ( tachycardia) can sometimes suddenly occur. The 3 different types of tachycardias associated with accessory pathways are shown in Figure 3.

The most common type (Figure 3 A) results from an electric circuit that travels from the atria through the AV node to the ventricles, then backward through an accessory pathway to the atria, and then back through the same circuit over and over again. Because this is a circuit that reenters itself and involves the atria and ventricles, it is referred to as AV reentrant tachycardia. The less common type of AV reentrant tachycardia (Figure 3 C) involves a circuit that travels forward from the atria through the accessory pathway and backward through the AV node.

Another type of tachycardia that can be seen in patients with accessory pathways is a chaotic irregular beating of the upper chambers of the heart called atrial fibrillation. If a patient with an accessory pathway develops atrial fibrillation and if that particular accessory pathway is capable of rapid electric conduction, this can lead to an extremely rapid pulse rate, which can be dangerous.

What is Wolff-Parkinson-White Syndrome?

Wolff-Parkinson-White syndrome (WPW) is the combination of accessory pathway activation seen on an ECG (delta waves) and episodes of tachycardia. It was first described in 1930 by Louis Wolff, Sir John Parkinson, and Paul Dudley White. Along with a delta wave, patients have a shorter time between the conduction of an impulse from the atrium to the ventricle, referred to as a short PR interval (see the ECG in Figure 2).

What is described above is called a preexcitation or WPW pattern. The presence of a pattern does not necessarily mean that the patient will experience WPW syndrome. The WPW pattern will be seen in about 0.2% of the general population. Of those patients with the WPW pattern, a minority will experience tachycardia and be defined as having WPW syndrome. WPW can be associated with Ebstein anomaly, a heart defect in which the valve connecting the right atrium and ventricle (tricuspid valve) is abnormally formed and placed lower than normal in the right ventricle. However, in most patients, WPW is not related to any other heart abnormality. It can occur at any age, is often first noted in childhood, but may not be diagnosed until adulthood in some patients. Symptoms of WPW syndrome are usually abrupt and may include palpitations, chest discomfort, and occasionally fainting.

On very rare occasions (less than 0.1% of the time), a patient with WPW can experience sudden cardiac death that results from the development of a chaotic irregular beating in the upper chambers of the heart called atrial fibrillation with rapid conduction down an accessory pathway (Figure 3B) leading to an extremely rapid pulse that can lead to cardiac arrest. Fortunately, this is a rare event in patients with WPW, and there are certain factors that a physician can often identify ahead of time to risk stratify patients with WPW.

Treatment

Treatment of WPW must be individualized. For patients who have only a documented WPW pattern on their ECG but no symptoms and no documented tachycardia, simple conservative observation may be appropriate. When symptoms or documentation of arrhythmias exists, a catheter-based electric evaluation of the heart called an electrophysiology study may be offered. This usually results in elimination of the accessory pathway with cautery delivered through the catheter called radiofrequency ablation. This will also eliminate the WPW pattern on the ECG. On rare occasions, WPW syndrome may be treated with antiarrhythmic medications, although most patients opt for the catheter ablation procedure because it may be curative and eliminate the need for lifelong medication therapy.

Conclusions

WPW syndrome results from tachycardia associated with an accessory pathway. The WPW pattern is diagnosed by a delta wave and/or short PR interval on an ECG. Once symptomatic, patients can be treated with catheter ablation or can try medications to control their symptoms. Management of WPW syndrome should be individualized, and treatment decisions should be carefully discussed with your doctor.

Reference: J.Kulig et al; Circulation 2010; 122: e480-e483.

 

Questions if you are considering a heart surgery!

Written by Dr. Hassan Gargoum on . Posted in Useful Information. No Comments on Questions if you are considering a heart surgery!

What to ask your cardiologist…

  • What   is coronary artery disease? How many heart vessels are blocked?

  • What   are my treatment options and what are the risks and benefits of each?

  • Why   are you recommending this treatment over the others?

  • What   lifestyle changes will I need to make and what community resources are   available to help?

  • If   I decide not to have open-heart surgery, will you support my decision?

  • Will   I be given some time to put my affairs in order prior to the heart surgery?

  • Should   I complete an Advance Directive?

  • Should   I avoid caffeine and other stimulants for 48 hours prior to surgery?

  • (If   diabetic) How often should I be monitoring my blood sugar?

  • If   I opt to have surgery, will I need to take medication afterwards? If so, for   how long?

What to ask your heart surgeon…

  • What   are the risks and complications associated with this surgery?

  • What   are my specific risks? How risky is my surgery?

  • Did   I have a heart attack? If so, how will this affect my surgery?

  • How   many other (men / women) have you operated on with my same condition and what   were their outcomes?

  • How   many patients do you operate on each year? How many of your patients were   women?

  • Can   my chest and leg scars be minimized or can vessels be taken from a less   visible location?

  • How   long is my expected recovery? When will I be able to resume normal   activities? Drive a car? Return to work? Have sex? Be independent in   activities of daily living? Make plans for help in the home for the first   full two weeks following your discharge from the hospital. Ask for a social   service referral to help assist your family with sharing duties.

  • What   is your fee? Will you accept my insurance as payment in full?

  • If   I decide not to have blood products administered, does the hospital follow   Bloodless Care Protocols?

  • What   accommodations are available for my family’s stay on the hospital campus so   that they can support me throughout the operation?

  • When   will you be available to answer some of my concerns about the operation? Write   down your appointment time to speak with your surgeon or the cardiac team   nurse:Date _________ Time__________

Tell your heart surgeon…

  • If   you want bloodless care;

  • If   you want your Advance Directives postponed during surgery. This is the usual   procedure. It will be reinstated after you are stable and transferred to   intensive care;

  • If   you have had a vein stripping operation. The doctor will need to look   elsewhere for vessels;

  • If   you would like to hear reassurances during the operation that “all is   going well”;

  • If   you would like to employ holistic measures to help you relax, for example   therapeutic massage, aroma therapy, reflexology, bio-feedback or music   therapy.

  • If   you would like to play a relaxing CD during the surgery. You may need to   bring in your own headphones and CD player, but this may be well worth the   trouble.

Discuss with your anesthesiologist any health history that could   affect how you respond to anesthesia, for example, if you…

  • Have   panic attacks

  • Experience   chest pains not related to activity

  • Take   medication for anxiety

  • Excessively   drink, binge drink or do weekend drinking

  • Take   herbal supplements

  • If   you or a family member (blood relative) has ever had a serious reaction to   anesthesia;

  • If   you have a drug allergy or sensitivity or you are allergic to latex.

List drug allergies here:
 
  _____________________________________________________

Source: Women’s Health Foundation

Hypertrophic Cardiomyopathy (HCM)

Written by Dr. Hassan Gargoum on . Posted in Useful Information. No Comments on Hypertrophic Cardiomyopathy (HCM)

Hypertrophic cardiomyopathy is a condition where the heart muscle becomes thickened. The symptoms that develop depend on the severity of the condition. The treatment depends on the type of symptoms you have and whether complications develop. Some people need no treatment. Most cases are hereditary so screening of close family members is advised.

What happens in hypertrophic cardiomyopathy?

In HCM the heart muscle becomes thickened (hypertrophies) in parts of the heart. In the normal heart, the muscle cells are regular and patterned. In HCM the cells of the heart muscle become irregular and disordered.

The muscle surrounding the left ventricle is the area commonly affected. Sometimes the muscle around the right ventricle is also affected. The degree of thickening may vary in different places. For example, the septum (the wall dividing the right and left ventricle) is often the area with the greatest thickening. In about 1 in 4 people the muscle thickening is evenly distributed throughout the walls of the left ventricle.

The thickened heart muscle usually contracts well to pump blood out of the heart. However, it may lead to problems which include the following:

  • The affected heart muscle (usually around the left ventricle) may become stiff. This can mean that your left ventricle may not fill as  easily as normal. Less blood than normal is then pumped out from your heart with each heartbeat.
  • The thickening is often most marked in the upper part of the septum. This may partly obstruct the flow of blood from your left  ventricle into your aorta. This results in less blood being pumped out from your heart.
  • The thickened heart muscle may affect the function of your heart  valves. In particular, the mitral valve may become leaky if it does not close properly.
  • In some people, the abnormal heart muscle affects the electrical conducting system of the heart. This may cause abnormal heart rates and/or rhythms to develop.

What causes hypertrophic cardiomyopathy?

Heart muscle can thicken because of something, such as high blood pressure. In HCM the heart muscle thickens without an obvious cause.

In most cases the condition is inherited. If a couple (where one person has HCM) has a child, there is a 1 in 2 chance of the child being affected. This pattern of inheritance is called autosomal dominant. It seems that affected people inherit defective genes which are involved in making parts of the heart muscle cells.

Men and women are affected equally.

Who develops hypertrophic cardiomyopathy?

It is sometimes present at birth and can develop in young children. However, it most commonly develops in the teenage years or early adulthood.

What are the symptoms of hypertrophic cardiomyopathy?

If you only have mild thickening of the heart muscle you may not have any symptoms. Symptoms can range from mild to severe and may not develop straight away. Possible symptoms include the following:

  • Shortness of breath. This may develop only when you exercise if the condition is mild. When the condition is more severe, you can be breathless at rest.
  • Chest pain (angina). This may develop only when you exercise, but can also occur at rest when it is more severe. The pain occurs because the supply of blood and oxygen to the heart muscle is not sufficient to meet the demands of the thickened muscle.
  • Palpitations. Sometimes abnormalities of heart rhythm (arrhythmias) develop which can cause palpitations. You      may become aware that your heartbeat is fast and/or irregular.
  • Dizziness and fainting attacks. These occur more commonly when you exercise, but may occur when you are resting. This may be due to reduced output of blood from the heart or because of arrhythmias.

How is hypertrophic cardiomyopathy diagnosed?

A doctor may suspect this condition because of:

  • Your symptoms.
  • Your family history.
  • Changes on your electrocardiogram (ECG) – this is a tracing of the electrical activity of the heart.
  • Changes on your chest X-ray. This may show your heart is large or that there is fluid in your lungs.
  • Ultrasounds scan of the heart. This is called an echocardiogram.   This is a painless test which can measure the thickness of your heart      muscle.

Once the diagnosis is confirmed, other tests may be needed to assess the severity of your condition. A Doppler ultrasound scan also looks at blood flow through the heart chambers. This shows how well the heart ventricles are filling and contracting. A Doppler ultrasound scan can also show if there is any turbulent blood flow within the ventricles.

How does the condition progress?

The thickening of the heart muscle does not tend to progress once you stop growing. This means that, for many people, the symptoms remain stable during adulthood. Unfortunately, the symptoms gradually become worse for some people as the heart muscle becomes stiffer. Sometimes the function of the heart gradually deteriorates and heart failure may develop.

Complications may occur and include the following:

Arrhythmias

An arrhythmia is an abnormal rate or rhythm of the heartbeat. There are various types of arrhythmia, some more serious than others. Sometimes an arrhythmia develops intermittently and can cause bouts of palpitations, dizziness and other symptoms. Some arrhythmias become permanent. Arrhythmias can usually be treated.

Endocarditis

This is a rare complication. Endocarditis is an infection of the inside lining of the heart chambers and heart valves. Unless promptly treated, endocarditis can cause serious illness.

People with HCM used to be advised to take antibiotics before dental treatment or other procedures. This is no longer the case, as taking antibiotics has not been shown to reduce the risk of developing infective endocarditis.

Sudden death

Sudden collapse and death occurs in a small number of people with HCM. This is probably due to a severe arrhythmia which may develop suddenly. People most at risk are those with more severe disease, especially those who have had a previous serious arrhythmia. Some people at high risk may be advised on treatments which aim to prevent or treat arrhythmias.

What is the treatment for hypertrophic cardiomyopathy?

There is no treatment which can reverse the changes of the heart muscle. Treatment aims to ease symptoms if they occur and to prevent complications. If you do not have any symptoms or you only have mild symptoms then you may not need any treatment. Treatment which may be required includes the following:

Medication

The medicines advised depend on what symptoms or complications develop. For example:

  • Beta-blockers (such as propranolol)      and calcium antagonists (especially verapamil) are the commonly used  medicines. These can slow the heart rate and make the heart contract less  forcefully. This allows more time for the ventricle to fill with each  heartbeat. These medicines may be used to treat chest pain, breathlessness and palpitations.
  • Various other medicines called anti-arrhythmic medicines (for example, amiodarone) are used to treat and to prevent arrhythmias.   They work by interfering with and helping to correct the electrical  impulses in your heart.
  • Warfarin may be advised if you  develop atrial fibrillation (a common arrhythmia). With this arrhythmia a blood clot is a possible complication. Warfarin is an anticoagulant. This means it helps to prevent blood clotting by thinning the blood.

Other types of treatment for arrhythmias

Other treatments may be an option if you develop arrhythmias. For example:

  • Cardioversion is an option for some types of arrhythmia. Whilst under anaesthetic, you are given an electric shock over the heart. This may revert the rhythm back to normal.
  • Artificial pacemakers are used in certain types of arrhythmia where the heart beats abnormally slowly (complete heart block) and in certain other situations. An artificial pacemaker is a small device which is inserted just under the skin on the upper chest.  Wires from the pacemaker are passed through veins into the heart chambers.  The pacemaker can then stimulate the heart to maintain a regular normal heartbeat.
  • Implantable cardioverter defibrillators (ICDs) are sometimes used in certain situations – especially if you are at risk of developing serious and life-threatening arrhythmias. They are small devices which are similar to pacemakers and are inserted under the  skin in the upper chest. Wires are passed through a vein to the heart. The device monitors the heartbeat. If it detects an abnormal rhythm, the device can send a small electrical shock to the heart to change it back to normal.

Surgery

If your cardiomyopathy is severe, an operation may be option:

  • Myectomy. This is an operation to remove a segment of thickened muscle from the septum. It is done as open  heart surgery. It is not a cure, but can help if the thick septum is causing obstruction to the flow of blood through the aortic valve.
  • Alcohol septal ablation. This is a fairly new technique. Alcohol is injected into the small arteries which supply the thickened area of heart muscle. This destroys that part of muscle, which then becomes thinner.
  • Valve replacement may be needed if the mitral valve is affected and does not work properly.
  • A heart transplant may be needed in a small number of people.

Some other general points

  • Family testing (screening). Your first-degree relatives (mother, father, brother, sister, child) should have tests such as a heart tracing and an echocardiogram. Some people with HCM do not have any symptoms. This is why close relatives should be screened. People with HCM have a 1 in 2 chance of passing the condition on to their children. In some centers it may be possible to have a genetic blood test.
  • Exercise. Depending on the severity of the condition, some people are advised not to take part in strenuous sports or jobs. Your doctor can advise you about this.
  • Weight. Try not to become  overweight, which can put an extra strain on your heart.
  • Alcohol. Normal social drinking  in moderation should not affect your heart. However, too much alcohol can affect the heart muscle and should be avoided.

 Source: patient.co.uk