ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executive summary.
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Adult↗
Biomedical subjects
Sidney Goldstein
Publications and source records attributed to Sidney Goldstein.
Effects of pre-existing left ventricular hypertrophy on ventricular dysfunction and remodeling following myocardial infarction in rats.
BACKGROUND: Myocardial hypertrophy is a characteristic component of left ventricular (LV) remodeling that may, at least initially, have a beneficial effect on LV function following myocardial infarction (MI). In the present study, we examine the effects of pre-existing left ventricular hypertrophy (LVH) on LV function and chamber enlargement following MI in inbred Lewis rats. METHODS: The one-kidney, one-clip model (1K1C) of hypertension was used to produce LVH. Four weeks after 1K1C, rats were randomized to left anterior descending coronary artery ligation (LVH + MI group, n = 8) or sham ligation (LVH group, n = 11). Another group of rats underwent sham 1K1C. Four weeks later, they were randomized to coronary ligation (MI group, n = 12) or sham ligation (Sham group, n = 12). LV end-diastolic pressure (EDP, mm Hg), end-diastolic volume (EDV, ml), end-systolic volume (ESV, ml) and ejection fraction (EF) (determined by angiography) were measured in all groups 2 months after MI. RESULTS: LV EDP was 20 +/- 2 mm Hg in the LVH + MI group compared with 9 +/- 1 mm Hg in the MI group (p < 0.05). LV EDV and ESV were significantly greater with LVH + MI than with MI alone (EDV 0.90 +/- 0.03 vs 0.75 +/- 0.02 ml; ESV 0.68 +/- 0.02 vs 0.50 +/- 0.03 ml; p < 0.05). Pre-existing LVH resulted in a greater reduction in EF following MI (25 +/- 2% for LVH + MI vs 34 +/- 2% for MI alone; p < 0.05). CONCLUSIONS: Pre-existing LVH is an important determinant of progressive LV dysfunction and remodeling following MI in Lewis inbred rats.
Animals↗
Sudden death in heart failure: underlying electrophysiological mechanisms.
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Action Potentials↗
Effects of chronic neutral endopeptidase inhibition on the progression of left ventricular dysfunction and remodeling in dogs with moderate heart failure.
BACKGROUND: The diuretic actions of endogenously produced atrial natriuretic factor (ANF) may be beneficial in the treatment of chronic heart failure (CHF). Neutral endopeptidase (NEP) is the primary enzyme responsible for the degradation of ANF. The present study investigates the effects of long-term NEP inhibition on the progression of left ventricular (LV) dysfunction and remodeling in dogs with moderate heart failure. METHODS: LV dysfunction was produced in 12 dogs by multiple sequential intracoronary microembolizations. Embolizations were discontinued when LV ejection fraction (EF) was between 30-40%. Two weeks after the last embolization, dogs were randomized to 3 months of oral therapy with the NEP inhibitor ecadotril (100 mg, once daily, n = 6) or to no therapy at all (control, n = 6). RESULTS: During the 3 months of follow-up, LV EF in control dogs decreased from 37 +/- 1% to 28 +/- 1% (P < 0.01) and LV end-diastolic volume (EDV) and end-systolic volume (ESV) increased (EDV: 72 +/- 3 vs. 84 +/- 5 ml, P < 0.01); ESV: 45 +/- 1 vs. 60 +/- 4 ml, P < 0.01). In dogs treated with ecadotril, LV EF (34 +/- 1% vs. 37 +/- 2%), EDV (79+/- 5 vs. 78+/- 6 ml) and ESV (52 +/- 3 vs. 49 +/- 4) remained essentially unchanged after 3 months of therapy. Histomorphometric measurements at the termination of the study showed that ecadotril was associated with significantly reduced cardiomyocyte hypertrophy compared to control. CONCLUSION: Early, long-term NEP inhibition with ecadotril prevents the progression of LV dysfunction and attenuates progressive LV remodeling in dogs with moderate heart failure.
Animals↗
Effects of long-term monotherapy with metoprolol CR/XL on the progression of left ventricular dysfunction and remodeling in dogs with chronic heart failure.
We examined the effects of long-term monotherapy with the beta-blocker, metoprolol controlled release/extended release (CR/XL), on the progression of LV dysfunction as well as on global and cellular remodeling in dogs with heart failure (HF). Chronic HF was produced by intracoronary microembolizations that were discontinued when LV ejection fraction (EF) was between 30% and 40%. Dogs were randomized to 3 months oral monotherapy with metoprolol CR/XL (100 mg once daily, n = 7) or no therapy at all (control, n = 7). In control dogs, EF decreased from 38 +/- 1% to 31 +/- 2% (p = 0.002), and LV end-systolic volume (ESV) and LV end-diastolic volume (EDV) increased (37 +/- 2 vs 45 +/- 2 ml, p = 0.001; 59 +/- 3 vs 65 +/- 3 ml, p = 0.001; respectively) during the 3 month follow-up period. In dogs treated with metoprolol CR/XL, EF increased after 3 months from 36 +/- 1% to 43 +/- 1% (p = 0.001), and ESV decreased (42 +/- 2 vs 38 +/- 2 ml, p = 0.003), whereas EDV remained unchanged. Compared to controls, treatment with metoprolol CR/XL showed 46% reduction in replacement fibrosis, 54% reduction in interstitial fibrosis and 20% reduction in myocyte cross-sectional area, a measure of myocyte hypertrophy. These findings indicate that metoprolol CR/XL improves LV function and attenuates progressive global and cellular LV remodeling in dogs with HF. The benefits are fully attributable to beta-blockade alone as no other adjunctive therapy was used.
Adrenergic beta-Antagonists↗
Beta blockers as cardioprotective agents: Part II--Focus on prevention of sudden cardiac death.
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Adrenergic beta-Antagonists↗
Debate: Do all patients with heart failure require automatic implantable defibrillators for the prevention of sudden death?
Recent clinical trials indicate that approximately two-thirds of patients in New York Heart Association (NYHA) class II and III, who comprise almost 90% of patients with heart failure, die suddenly. Patients in NYHA class IV usually die of progressive heart failure. Implantation of implantable cardioverters defibrillators (ICDs) in this population would represent a huge logistic problem and economic expense. Clinical trials have recently demonstrated that beta-blocker therapy with carvedilol, bisoprolol, and toprol XL decrease the sudden death rate by almost 50%, in addition to impacting significantly on death due to worsening heart failure. This medical approach is beneficial to all patients, and should be our major therapy. However, it is reasonable to attempt to identify that subpopulations of heart failure patients who could benefit from an ICD.
Journal Article↗
The COMET trial.
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Adrenergic beta-Antagonists↗