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We reviewed the records of 242 patients admitted over 1 year with heart failure and an ejection fraction < or = 45% to assess the use of angiotensin-converting enzyme inhibitors. Most patients were treated with angiotensin-converting enzyme inhibitors. However, an important minority (8%) had no apparent reason for the lack of this treatment, highlighting the need for strategies to increase the use of these beneficial agents.
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The new finding was that mean heart rate and heart rate variability were more closely coupled in patients with more advanced LV dysfunction. Mean heart rate explained a larger portion of variance in heart rate variability in patients in the lowest LVEF quartile than in those in the highest one. These results support our hypothesis that sympathetic activation in patients with more severe LV dysfunction results in closer correlation between heart rate and heart rate variability. Generally, the correlation between mean heart rate and heart rate variability is weak because heart rate and heart rate variability represent different modalities of cardiovascular regulation. Mean heart rate is normally determined by the interactions of both the sympathetic and parasympathetic nervous systems, whereas modulation of these activities, with different gains, determines the magnitude of heart rate variability. This results in great complexity in control of the heart by the autonomic nervous system. However, heart rate is likely to be more dominantly regulated by the sympathetic nervous system because of vagal withdrawal in patients with more severe LV dysfunction. The effect of sympathetic cardiac modulation has been shown to be more sluggish than that of the parasympathetic nervous system in beat-to-beat regulation of heart rate. This may result in more blunted heart rate variability concomitantly with elevated mean heart rate. Thus, variation in heart rate variability in any given mean heart rate is likely to be lower than in patients with more preserved LV function, and hence with more complex cardiac autonomic regulation with involvement of the parasympathetic nervous system. Indeed, even the slopes of regression lines between mean heart rate and heart rate variability were similar in the first and fourth LVEF quartile; the intercept of the regression line was significantly higher in the fourth quartile than in the first one. This further supports our hypothesis.
Maximal oral vasodilator therapy resulted in long-term reduction of initially elevated pulmonary vascular resistance in 10 of 13 patients with severe heart failure who tolerated inotrope-supported uptitration of afterload reduction. Eleven patients were unable to tolerate vasodilator therapy and required inotropic support for successful cardiac transplantation.
In patients with heart failure, carvedilol ameliorated cardiac function, but it did not affect oxygen uptake, kinetics, and ventilatory efficiency during 6-minute exercise at a constant 50-W workload. Persistence of respiratory incompetence may prevent improvement in submaximal oxygen uptake kinetics.
Nisoldipine is a dihydropyridine calcium entry blocker that inhibits contraction of vascular smooth muscle with a potency that is 2-3 times greater than its impact on myocardial contractility. In isolated human coronary arteries, tonic contractions induced by serotonin are inhibited by nisoldipine with a potency 10 times greater than that in internal mammary arteries and 1,000 times greater than that in electrically driven myocardium. In contrast, nifedipine had little effect and verapamil and diltiazem had none. In this article an hypothesis is reviewed that relates vascular smooth muscle selectivity to membrane potential sensitivity. Nisoldipine's effect on calcium channel binding and blocking is enhanced by the degree of depolarization of the cell membrane. Verapamil and diltiazem are not membrane-potential sensitive. Vascular smooth muscle cells are more depolarized than myocardial cells, and human coronary arteries have a particularly small membrane potential. Thus, the potency of nisoldipine in these organs parallels the degree of membrane depolarization. This may then suggest ischemia selectivity, since membrane depolarization occurs in ischemic tissue. Nisoldipine might therefore have a potent negative inotropic effect and an enhanced vasodilator action in ischemic myocardium, yet leave normoxic regions functionally intact. Some experimental evidence is discussed.
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BACKGROUND: Preservation of the subvalvular apparatus has been demonstrated to be beneficial during first-time mitral valve replacement (MVR), but has not been fully examined in reoperative (redo) MVR. The purpose of this study was to analyze outcomes in a large cohort of redo MVR patients, focusing on the effect of subvalvular preservation on mortality. METHODS: We undertook a review of prospectively gathered data on patients undergoing MVR, with or without concomitant cardiac procedures, at our institution from 1990 to 1999. Predictors of mortality were determined by stepwise logistic regression. RESULTS: A total of 1,521 consecutive MVR patients were analyzed, of which, 513 (34%) had undergone one or more previous MV procedures. In-hospital mortality occurred in 6.9% of first-time MVR patients versus 9.0% in redo patients (p = 0.13). The number of prior MV operations ranged from one to five in redo MVR patients, with 115 patients (22% of redos) having two or more. In redo MVR patients, preservation of the native posterior subvalvular apparatus was performed in 103 patients (21%), whereas native anterior and posterior preservation was performed in 31 patients (6%). Gore-Tex neochordal construction was performed in 135 redo MVR patients (26%). Perioperative mortality occurred in 3.6% of redo MVR patients with a preserved subvalvular apparatus (native tissue and/or Gore-Tex reconstruction) versus 13.3% of redo patients without preservation (p < 0.001). Independent predictors of mortality in redo MVR patients were (in decreasing order of magnitude) failure to preserve the subvalvular apparatus, preoperative renal failure, previous stroke/transient ischemic attack, left ventricular dysfunction (left ventricular ejection fraction <40%), and urgent timing. CONCLUSIONS: Redo MVR can be performed with an acceptable risk of mortality. Although preservation of the subvalvular apparatus may increase operative complexity, we recommend subvalvular preservation in order to decrease the risk of early mortality.
BACKGROUND: Diabetes is a well-established risk factor for coronary artery disease, and it is associated with an increased rate of early and late adverse events after myocardial revascularization by coronary artery bypass grafting. METHODS: A prospective follow-up study was done to evaluate the short-term and mid-term outcomes of type II diabetic patients who had coronary artery bypass grafting at our institution between 1996 and May 1999. A total of 200 patients, 100 insulin-dependent diabetic patients (group I) and 100 non-insulin-dependent diabetic patients (group II), met the inclusion criteria of the study and were included in the clinical follow-up study. RESULTS: The characteristics of the patients of the two groups were similar for baseline clinical angiographic and operative characteristics. In particular, no significant differences in cardiopulmonary bypass and aortic cross-clamping times were noted between the two groups. The number grafts per patient was similar between the two groups. There were no in-hospital deaths, but postoperative complications were different among the two series. In fact, 33% of patients in group I had at least one major complication compared with 20% in group II (p = 0.037). The cumulative number of complications was 148 in group I and 69 in group II, and the mean number of complications per patient was 4.5 and 3.5 in groups I and II, respectively. The major differences in perioperative complication rates were found in the need for prolonged (> 24 hours) ventilation, occurrence of respiratory or renal insufficiency, and mediastinitis. The mean length of stay in the intensive care unit and for total hospitalization were longer in group I than group II (4.3 +/- 2.8 days versus 2.8 +/- 2.7 days [p = 0.010] and 11.1 +/- 2.2 days versus 7.2 +/- 2.4 group II [p < 0.05], respectively). At long-term follow-up, group I patients had a significantly higher mortality rate (29% versus 10%, p < 0.001). Moreover, overall late cardiac and noncardiac complication rates were significantly higher in group I than II (37% versus 22%, p = 0.02). In the multivariate analysis including several preoperative and operative variables, treatment by insulin, advanced age (> 75 years), left ventricular dysfunction (left ventricular ejection fraction < 35%), and complex lesions at coronary angiography (American Heart Association lesion classification type C lesion) were found as independent predictors of increased mortality. CONCLUSIONS: Our data show that patients with insulin-dependent type II diabetes who had coronary artery bypass grafting have a significantly higher rate of major postoperative complications with an extremely unfavorable short- and long-term prognosis. Diabetic patients on insulin treatment should be considered high-risk candidates for coronary artery bypass grafting and require intense perioperative and long-term monitoring. Further studies will be necessary to investigate whether such conclusions may be appropriate for newer surgical strategies such as off-pump operation.
BACKGROUND: The use of the intraaortic balloon pump (IABP) in patients undergoing coronary artery bypass grafting has been traditionally associated with a high complication rate and adverse outcomes. However, recent reports show that many of these catastrophic outcomes can be avoided by preoperatively placing the IABP in high-risk patients. To further validate these reports, we defined a set of liberal criteria for preoperative IABP insertion and applied them to a series of elderly patients (70 years or older) undergoing isolated coronary artery bypass grafting. METHODS: Two hundred six consecutive patients who underwent isolated coronary artery bypass grafting with cardiopulmonary bypass were retrospectively reviewed. A rapid recovery protocol emphasizing reduced cardiopulmonary bypass time, an anesthetic protocol for early extubation, perioperative administration of corticosteroids and thyroid hormone, and aggressive diuresis was applied to all patients. Patients who required an urgent operation because of failed percutaneous transluminal coronary angioplasty, a critical left main stenosis (70% or greater), pronounced left ventricular dysfunction (left ventricular ejection fraction 40% or less), or unstable angina refractory to medical therapy or who required an emergency reoperation received preoperative IABP support. RESULTS: The 30-day mortality rate for the entire group was 4.4%. There were 97 patients (47%) who received a preoperative IABP (group II) in comparison with 109 patients (53%) who did not fulfill the preoperative insertion criteria (group I). Patients in group II had a lower left ventricular ejection fraction (mean, 46% versus 59%, p<0.001) and a higher incidence of congestive heart failure (35% versus 17%, p<0.01) and acute myocardial infarction (37% versus 17%, p<0.01) than patients in group I. The average postoperative hospital length of stay for patients in group II was slightly longer than for those in group I (9.0+/-10.5 versus 6.0+/-3.7 days, p<0.01). However, there were no statistically significant differences in complication or mortality rates between the two groups. Only 2 patients (2.2%) had complications related to IABP insertion. Lower extremity ischemia occurred in both patients, and both were treated successfully with thromboembolectomy. CONCLUSIONS: Liberal preoperative insertion of the IABP can be performed safely in high-risk elderly patients undergoing coronary artery bypass grafting, with results comparable to those in lower risk patients.
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OBJECTIVES: Our purpose was to evaluate the long-term benefit of myocardial viability assessment for stratifying risk and selecting patients with low ejection fraction for coronary artery bypass grafting and to determine the relation between the severity of anginal symptoms, the amount of ischemic myocardium, and clinical outcome. METHODS: We studied 93 consecutive patients with severe coronary artery disease and low ejection fraction (median, 25%) who underwent positron emission tomography to delineate the extent of perfusion-metabolism mismatch (reflecting hibernating myocardium) for potential myocardial revascularization. Median follow-up was 4 years (range, 0 to 6.2 years). RESULTS: Fifty patients received medical therapy, and 43 patients underwent bypass grafting. In Cox survival models, heart failure class, prior myocardial infarction, and positron emission tomographic mismatch were the best predictors of survival. Patients with positron emission tomographic mismatch receiving bypass grafting had improved 4-year survival compared with those on medical therapy (75% versus 30%; P =.007) and a significant improvement in angina and heart failure symptoms. In patients without positron emission tomographic mismatch, bypass grafting tended to improve survival and symptoms only in those patients with severe angina (100% versus 60%; P =.085), whereas no survival advantage was apparent in patients with minimal or no anginal symptoms (63% versus 52%; P =.462). CONCLUSIONS: Patients with low ejection fraction and evidence of viable myocardium by positron emission tomography have improved survival and symptoms with coronary bypass grafting compared with medical therapy. In patients without evidence of viability, survival and symptom improvement with bypass grafting are apparent only among those patients with severe angina.