Postinfarction Chronic Heart Failure Research Articles

Treatment with growth hormone enhances contractile reserve and intracellular calcium transients in myocytes from rats with postinfarction heart failure.

Recombinant human growth hormone (GH) improves in vivo cardiac function in rats with postinfarction heart failure (MI). We examined the effects of growth hormone (14 days of 3.5 mg. kg-1. d-1 begun 4 weeks after MI) on contractile reserve in left ventricular myocytes from rats with chronic postinfarction heart failure. Cell shortening and [Ca2+]i were measured with the indicator fluo 3 in myocytes from MI, MI+GH, control, and normal animals treated with GH (C+GH) under stimulation at 0.5 Hz at 37 degrees C. Cell length was similar in MI and MI+GH rats (150+/-5 and 157+/-5 microm) and was greater in these groups than in the control and C+GH groups (140+/-4 and 139+/-4 microm, P<0.05). At baseline perfusate calcium of 1.2 mmol/L, myocyte fractional shortening and [Ca2+]i transients were similar among the 4 groups. We then assessed contractile reserve by measuring the increase in myocyte fractional shortening in the presence of high-perfusate calcium of 3.5 mmol/L. In the control and C+GH groups, myocyte fractional shortening and peak systolic [Ca2+]i were similarly increased in the presence of high-perfusate calcium. In the presence of high-perfusate calcium, both myocyte fractional shortening and peak systolic [Ca2+]i were depressed in the MI compared with the control groups. In contrast, myocyte fractional shortening (14.1+/-.9% versus 11.1+/-.9%, P<0.05) and peak systolic [Ca2+]i (647+/-43 versus 509+/-37 nmol/L, P<0.05) were significantly higher in MI+GH than in MI rats and were comparable to controls. Left ventricular myocyte expression of sarcoplasmic reticulum Ca2+ ATPase 2 (SERCA-2) and left ventricular SERCA-2 protein levels were increased in MI+GH compared with MI rats. Calcium-dependent contractile reserve is depressed in myocytes from rats with postinfarction heart failure. Long-term growth hormone therapy increases contractile reserve by restoring normal augmentation of systolic [Ca2+]i in myocytes from rats with postinfarction heart failure.

Restoration of Regional Wall Motion by Nitroglycerin Therapy in Patients with Left Ventricular Asynergy

A ortocoronary bypass operation has a variable effect on the function of the left ventricle. 1 Bourassa MG L’Esperance J Campeau L et al. Fate of left ventricular contraction following aorto-coronary venous grafts. Early and late post-operative modifications. Circulation. 1972; 46: 724-730 Google Scholar , 2 Chatterjee K Swan HJC Parmley WW et al. Influence of direct myocardial revascularisation on left ventricular asynergy and function in patients with coronary heart disease.. Circulation. 1973; 47: 276-286 Crossref PubMed Scopus (216) Google Scholar , 3 Rees G Bristow JD Kremkau EL et al. Influence of aorto-coronary bypass surgery on left ventricular performance.. N Engl J Med. 1971; 284: 1116-1121 Crossref PubMed Scopus (141) Google Scholar This may be due, in part, to inability to predict the behavior of regional wall abnormalities following revascularization. Areas of asynergy may have pronounced influence on left ventricular function, 4 Herman MV Heinle RA Klein MD et al. Localized disorders in myocardial contraction: Asynergy and its role in congestive heart failure.. N Engl J Med. 1967; 277: 222-232 Crossref PubMed Scopus (404) Google Scholar , 5 Baxley WA Jones WD Doslye HT Left ventricular anatomical and functional abnormalities in chronic postinfarction heart failure.. Ann Intern Med. 1971; 74: 499-508 Crossref PubMed Scopus (27) Google Scholar and yet traditional hemodynamic techniques measure the integrated response of the left ventricle as though all segments made a uniform contribution to total function. Previous investigations show that abnormal wall motion occurs in zones supplied by those arteries with critical stenosis. 6 Sniderman AD Marpole D Fallen EL Regional contraction patterns in the normal and ischemic left ventricle in man.. Am J Cardiol. 1973; 31: 484-489 Abstract Full Text PDF PubMed Scopus (72) Google Scholar , 7 Gorlin R Klein MD Sullivan JM Prospective correlative study of ventricular aneurysm with special reference to mechanistic concept and clinical recognition.. Am J Med. 1967; 42: 512-531 Abstract Full Text PDF PubMed Scopus (198) Google Scholar

Left ventricular anatomical and functional abnormalities in chronic postinfarction heart failure.

Fifty patients with chronic postmyocardial infarction heart failure had quantitative biplane angiocardiography; 42 also had coronary angiography. Mitral regurgitation, localized ventricular contraction abnormality, increased end-diastolic volume, low ejection fraction, low cardiac index, and high left ventricular end-diastolic pressure occurred in various combinations. Mitral regurgitation averaged 2.11 liter/min per m2 body surface area and occurred most commonly with right coronary occlusion, low cardiac index or elevated left ventricular end-diastolic pressure or both, and left ventricular end-diastolic volumes exceeding 155 ml/m2 body surface area. End-diastolic volumes were increased in 86% and ranged to 450 ml/m2 body surface area. Ejection fractions were below 0.50 in 92%. Coronary angiographic findings correlated poorly with ventricular hemodynamic values. Localized contraction abnormalities included aneurysms with up to 40 ml per stroke paradoxical blood flow. Localized contraction abnormalities were not significantly more frequent in patients with low cardiac indexes or elevated left ventricular end-diastolic pressure, or both. High ventricular filling pressure or a low cardiac index, or both, was not commoner with multiple than with single vessel disease.

Surgical intervention in chronic postinfarction cardiac failure.

Seven patients with severe, chronic postmyocardial infarction cardiac failure underwent open intracardiac operation following catheterization and quantitative biplane angiocardiographic studies. Four patients with mitral incompetence had valve replacements; three had dilated mitral rings and did not survive the immediate postoperative period. In contrast, the single surviving patient had papillary muscle dysfunction evident at surgery and had less severe myocardial impairment as indicated preoperatively by a lower end-diastole volume and higher ejection fraction. Three patients demonstrated significant clinical and hemodynamic improvement after resection of a sccared akinetic area of left ventricular myocardium. Although two of the three patients died within the first year of operation, neither died in congestive failure. The results of this study indicate that certain patients with chronic postinfarction heart failure may benefit from surgery.