Revascularization in Severe Left Ventricular Dysfunction

AbstractThe highest-risk patients with heart failure with reduced ejection fraction are those with ischemic cardiomyopathy and severe left ventricular systolic dysfunction (ejection fraction ≤35%). The cornerstone of treatment is guideline-driven medical therapy for all patients and implantable device therapy for appropriately selected patients. Surgical revascularization offers the potential for improved survival and quality of life, particularly in patients with more extensive multivessel disease and the greatest degree of left ventricular systolic dysfunction and remodeling. These are also the patients at greatest short-term risk of mortality with coronary artery bypass graft surgery. The short-term risks of surgery need to be balanced against the potential for long-term benefit. This review discusses the evolving data on the role of surgical revascularization, surgical ventricular reconstruction, and mitral valve surgery in this high-risk patient population

Effects of regional systolic asynchrony on left ventricular global diastolic function in patients with coronary artery disease

AbstractPatients with coronary artery disease often have impaired left ventricular diastolic filling despite normal global systolic function. The influence of regional systolic asynchrony on diastolic function was assessed by radionuclide angiography in 60 patients with coronary artery disease and normal ejection fraction at rest: group 1 (n = 30) with normal wall motion at rest and group 2 (n = 30) with abnormal wall motion. Data were compared with those obtained from 19 normal volunteers.Age, heart rate, ejection fraction and echocardiographic enddiastolic dimension did not differ among the three groups. Peak filling rate in group 1 and group 2 was similar (2.5 ± 0.5 and 2.3 ± 0.6 end-diastolic counts/s, respectively) and significantly lower than that in the normal subjects (2.8 ± 0.7 end-diastolic counts/s; p < 0.01 vs. group 2, p < 0.05 vs. group 1). Time to peak filling rate was prolonged in group 2 (184 ± 27 ms) compared with that in normal subjects (162 ± 19 ms; p < 0.01) and group 1 (172 ± 15 ms; p < 0.05). Left ventricular end-diastolic pressure was significantly higher in group 2 than in group 1 (14 ± 7 vs. 10 ± 5 mm Hg, respectively; p < 0.05).Asynchrony was assessed by sector analysis of the radionuclide left ventricular region of interest. Diastolic asynchrony was similar in the two patient groups (30 ± 23 ms in group 2, 26 ± 16 ms in group 1) and was higher in both groups than in the normal subjects (16 ± 8 ms; p < 0.61). However, systolic asynchrony was higher in group 2 (32 ± 15 ms) than in both group 1 (14 ± 6 ms; p < 0.01) and the normal group (9 ± 6 ms; p < 0.01). In the total group of patients with coronary artery disease, systolic asynchrony correlated with global time to peak filling rate (r = 0.53; p < 0.001). This correlation became stronger when only group 2 was considered (r = 9.62; p < 0.001). Moreover, in group 2 systolic asynchrony correlated with the duration of the isovolumetric relaxation period (r = 0.58; p < 0.001) and the isovolumetric relaxation period, in turn, correlated with global time to peak filling rate (r = 0.72; p < 0.001).Thus, left ventricular systolic asynchrony affects both the relaxation and filling phases of diastole, thereby contributing to the impairment of diastolic function commonly observed in patients with coronary artery disease

Comparative effects of verapamil and nitroprusside on left ventricular function in patients with hypertension

AbstractThe effects of verapamil were compared with those of nitroprusside at matched mean arterial pressures and heart rates in 10 symptomatic hypertensive patients during cardiac catheterization. Simultaneous radionuclide angiography and micromanometer pressure measurements were obtained to assess left ventricular pressure-volume relations. Compared with control conditions, verapamil increased left ventricular end-diastolic volume index from 57 ± 16 to 70 ± 28 ml/m2 (p = 0.05) without a significant increase in left ventricular end-diastolic pressure (from 10 ± 4 to 13 ± 6 mm Hg). Despite a downward and rightward shift in the end-systolic pressure-volume relation indicating negative inotropic effects, ejection fraction did not decrease significantly (from 52 ± 9% to 46 ± 9%); cardiac index and stroke volume index remained unchanged. The change in stroke volume index with verapamil was directly related to the magnitude of change in end-diastolic volume index (r = 0.82, p < 0.005), suggesting that the increase in enddiastolic volume did not arise purely from negative inotropic effects. Systemic vascular resistance index decreased from 42 ± 8 to 34 ± 7 mm Hg-min-m2/liter (p < 0.05).In contrast, nitroprusside decreased left ventricular end-diastolic volume index from 57 ± 16 to 41 ± 10 ml/m2 (p < 0.05), cardiac index from 3.2 ± 0.7 to 2.8 ± 0.6 liters/min per m2 (p < 0.05) and stroke volume index from 28 ± 6 to 24 ± 5 ml/m2 (p < 0.01), with no change in systemic vascular resistance index (40 ± 10 mm Hg·min·m2). The end-systolic pressure-volume relation shifted downward and leftward in all patients, stemming from altered left ventricular loading.Thus, in equihypotensive doses, verapamil and nitroprusside have markedly different effects on left ventricular function. The peripheral vasodilation and apparent improvement in left ventricular filling during verapamil balanced the negative inotropic effects, resulting in maintenance of stroke volume and cardiac index. The primary hypotensive effect of verapamil was a decrease in systemic vascular resistance, whereas that of nitroprusside was a decrease in cardiac index stemming from reduced left ventricular preload

Coronary-artery bypass surgery in patients with ischemic cardiomyopathy

BACKGROUND The survival benefit of a strategy of coronary-artery bypass grafting (CABG) added to guideline-directed medical therapy, as compared with medical therapy alone, in patients with coronary artery disease, heart failure, and severe left ventricular systolic dysfunction remains unclear. METHODS From July 2002 to May 2007, a total of 1212 patients with an ejection fraction of 35% or less and coronary artery disease amenable to CABG were randomly assigned to undergo CABG plus medical therapy (CABG group, 610 patients) or medical therapy alone (medical-therapy group, 602 patients). The primary outcome was death from any cause. Major secondary outcomes included death from cardiovascular causes and death from any cause or hospitalization for cardiovascular causes. The median duration of follow-up, including the current extended-follow-up study, was 9.8 years. RESULTS A primary outcome event occurred in 359 patients (58.9%) in the CABG group and in 398 patients (66.1%) in the medical-therapy group (hazard ratio with CABG vs. medical therapy, 0.84; 95% confidence interval [CI], 0.73 to 0.97; P=0.02 by log-rank test). A total of 247 patients (40.5%) in the CABG group and 297 patients (49.3%) in the medical-therapy group died from cardiovascular causes (hazard ratio, 0.79; 95% CI, 0.66 to 0.93; P=0.006 by log-rank test). Death from any cause or hospitalization for cardiovascular causes occurred in 467 patients (76.6%) in the CABG group and in 524 patients (87.0%) in the medical-therapy group (hazard ratio, 0.72; 95% CI, 0.64 to 0.82; P&lt;0.001 by log-rank test). CONCLUSIONS In a cohort of patients with ischemic cardiomyopathy, the rates of death from any cause, death from cardiovascular causes, and death from any cause or hospitalization for cardiovascular causes were significantly lower over 10 years among patients who underwent CABG in addition to receiving medical therapy than among those who received medical therapy alone. (Funded by the National Institutes of Health; STICH [and STICHES] ClinicalTrials.gov number, NCT00023595.

Metabolic evidence of viable myocardium in regions with reduced wall thickness and absent wall thickening in patients with chronic ischemic left ventricular dysfunction

AbstractReduced end-diastolic wall thickness with absent systolic wall thickening has been reported to represent nonviable myocardium in patients with chronic coronary artery disease. To assess whether reduced regional end-diastolic wall thickness and absent wall thickening accurately identify nonviable myocardium, 25 patients with ischemic left ventricular dysfunction (ejection fraction at rest 27 ± 10%) underwent positron emission tomography with oxygen-15-labeled water and 18fluorodeoxyglucose to assess metabolic activity and spin-echo gated nuclear magnetic resonance imaging to measure regional end-diastolic wall thickness and wall thickening. The presence of metabolic activity was defined as 18fluorodeoxyglucose uptake (corrected for partial volume) >50% of that in normal regions.Of 355 myocardial regions evaluated, 266 were hypokinetic or normokinetic at rest and 89 were akinetic (that is, absent wall thickening). 18Fluorodeoxglucose uptake was observed in 97% of the hypokinetic and normokinetic regions and in 74% of the akinetic regions. End-diastolic wall thickness was greater in akinetic regions with than in those without 18fluorodeoxyglucose uptake (11 ± 4 vs. 7 ± 3 nun, p < 0.01). The highest values for sensitivity and specificity of end-diastolic wall thickness in predicting the absence of metabolic activity in akinetic regions were 74% and 79%, respectively, and corresponded to an end-diastolic threshold of 8 mm. However, the positive predictive accuracy was only 55% and did not improve for other end-diastolic wall thickness values. In all myocardial regions, there was only a weak correlation between 18fluorodeoxyglucose activity and either end-diastolic wall thickness (r = 0.17) or wall thickening (r = 0.32).Thus, metabolic activity is present in many regions with reduced end-diastolic wall thickness and absent wall thickening. These data indicate that assessment of regional anatomy and function may be inaccurate in distinguishing asynergic but viable myocardium from nonviable myocardium