Month: September 2013

10 Key Points from the 2013 ESC Guidelines on the Management of Stable Coronary Artery Disease

10 Key Points from the 2013 ESC   Guidelines on the Management of Stable Coronary Artery Disease

 

These guidelines should be applied to patients with stable known or suspected coronary artery disease (SCAD). This condition encompasses several groups of patients: (i) those having stable angina pectoris or other symptoms felt to be related to coronary artery disease (CAD) such as dyspnoea; (ii) those previously symptomatic with known obstructive or non-obstructive CAD, who have become asymptomatic with treatment and need regular follow-up; (iii) those who report symptoms for the first time and are judged to already be in a chronic stable condition (for instance because history-taking reveals that similar symptoms were already present for several months). Hence, SCAD defines the different evolutionary phases of CAD, excluding the situations in, which coronary artery thrombosis dominates clinical presentation (acute coronary syndromes).

The following are 10 key points from the 2013 European Society of Cardiology guidelines for the management of stable coronary artery disease (CAD), with emphasis since the last guidelines publication in 2006:
1. There are different underlying mechanisms of stable known or suspected CAD (SCAD). These include fixed or dynamic plaque-related obstruction of epicardial arteries, focal or diffuse spasm of normal or plaque-disease arteries, microvascular dysfunction, and left ventricular dysfunction caused by prior acute myocardial necrosis and/or hibernation. These mechanisms allow for consideration of ‘microvascular dysfunction and coronary vasospasm in diagnostic and prognostic algorithms.’
2. Coronary computed tomography angiography (CTA) may be considered an alternative to ischemia testing, especially in patients with chest pain symptoms with low to intermediate pretest probability. While CTA should not be overused, its very high negative predictive value can provide reassurance in select circumstances.
3. Although promising and valuable in offering information on both overall cardiac anatomy and function in the same examination, magnetic resonance coronary angiography is still regarded as a research tool and is not officially recommended in the diagnostic evaluation of SCAD.
4. Cardiac rehabilitation, commonly offered after myocardial infarction or recent coronary intervention, should be considered in all patients with SCAD.
5. The treatment of microvascular angina includes optimal coronary risk factor control and traditional anti-ischemic therapy. Beta-blockers are recommended as first-line therapy, given their role in relieving effort-related angina.
6. Patients with a high pretest probability for CAD and/or severe symptoms may benefit from early invasive coronary angiography without noninvasive risk stratification.
7. Fractional flow reserve (FFR), intravascular ultrasound, and optical coherence tomography are methods of intracoronary assessment of coronary artery stenosis severity. The measurement of FFR during adenosine infusion may identify functionally significant stenosis and should be used frequently. A patient with a stenosis and an FFR >0.80 should not be revascularized.
8. While it has been well established that there is genetic variation to the response to antiplatelet therapy (especially clopidogrel) in patients with acute coronary syndrome or myocardial infarction, there are no established recommendations to perform genetic testing to guide treatment with antiplatelet therapy in patients with SCAD.
9. Ranolazone, a selective inhibitor of late sodium current, has anti-ischemic and metabolic properties. It is useful as add-on treatment for the management of stable angina in patients inadequately controlled by first-line therapy, and does not impact heart rate or blood pressure.
10. In light of the results of the FREEDOM trial, coronary artery bypass grafting may be the preferred revascularization strategy in diabetic patients with multivessel disease.

 

Source:   Cardiosource

 

 

Cardiac Resynchronization may be harmful in narrow-QRS heart failure

Cardiac-resynchronization therapy (CRT) reduces morbidity and mortality in chronic systolic heart failure with a wide QRS complex. Mechanical dyssynchrony also occurs in patients with a narrow QRS complex, which suggests the potential usefulness of CRT in such patients.

New data, from a randomized trial, presented at the European Society of Cardiology (ESC) 2013 Congress (also published in the New England Journal of medicine) concluded that cardiac resynchronization therapy (CRT) will not improve outcomes in patients with narrow QRS intervals (i.e.  <130 ms) and have evidence of ventricular dyssynchrony by echocardiographic criteria. In fact, it may actually increase the risk of cardiovascular death.

This  randomized trial involving 115 centers to evaluate the effect of CRT in patients with New York Heart Association class III or IV heart failure, a left ventricular ejection fraction of 35% or less, a QRS duration of less than 130 ms, and echocardiographic evidence of left ventricular dyssynchrony. All patients underwent device implantation and were randomly assigned to have CRT capability turned on or off. The primary efficacy outcome was the composite of death from any cause or first hospitalization for worsening heart failure.

At study closure, the 809 patients who had undergone randomization had been followed for a mean of 19.4 months. The primary outcome occurred in 116 of 404 patients in the CRT group, as compared with 102 of 405 in the control group (28.7% vs. 25.2%; hazard ratio, 1.20; 95% confidence interval [CI], 0.92 to 1.57; P=0.15). There were 45 deaths in the CRT group and 26 in the control group (11.1% vs. 6.4%; hazard ratio, 1.81; 95% CI, 1.11 to 2.93; P=0.02).

–       The primary end point had occurred in 218 patients with no significant difference between the two groups; however, there was a significant mortality increase in the CRT-on group (p=0.02).

–       There was no significant difference in changes in NYHA class from baseline to six months, nor were there differences in quality of life by the Minnesota Living with Heart Failure Questionnaire.

–       About 19% of CRT-on and 15.6% of CRT-off patients received ICD shocks, and significantly more CRT-on patients had inappropriate shocks, 5.0% vs 1.7% (p=0.01).

The authors concluded that in patients with systolic heart failure and QRS duration of less than 130 ms, CRT does not reduce the rate of death or hospitalization for heart failure and may increase mortality.

These findings shut down hopes that the usefulness of CRT might be extended to heart failure patients without significant QRS prolongation who have echo evidence of ventricular dyssynchrony.

The results of this study reinforce the notion that, at least until new methods of assessment are developed, QRS width (with or without mechanical dyssynchrony) remains the primary determinant of response to CRT. These data also suggest that CRT use in patients with QRS duration of less than 120 ms is unwarranted, could be harmful, and should not be considered. It also argues against the use of echocardiographic criteria for trying to identify patients with < 130 ms QRS duration who might respond to CRT.

Source:

–       Frank Ruschitzka, M.D., William T. Abraham, M.D., Jagmeet P. Singh, et al. Cardiac-Resynchronization Therapy in Heart Failure with a Narrow QRS Complex. NEJM; September 3, 2013DOI: 10.1056/NEJMoa1306687

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