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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Development of heart failure complicating acute myocardial infarction is directly related to the extent of myocardial infarction and complex architectural changes defined as infarct expansion and remodeling. ACE inhibitors are an exciting class of agents that have the potentiality to prevent left ventricular dilatation, evolution of heart failure and death in the acute myocardial infarction setting. Besides, reperfusion is a important intervention that prevents infarct expansion in the early period after myocardial infarction. Early reperfusion limits expansion by infarct size reduction while late reperfusion reduces expansion independent of myocardial salvage by limiting transmural damage and improving the infarct healing. Therefore, reperfusion therapy decreases the incidence of congestive heart failure and significantly improves the prognosis of heart failure. On the other hand, the in-hospital mortality rate of cardiogenic shock, resulting from acute myocardial infarction, remains high, although primary PTCA has apparently resulted in substantial improvement in mortality of myocardial infarction shock. Thus, reperfusion treatment may be more effective in preventing rather than treating cardiogenic shock.
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PMID:[Management of heart failure complicating acute myocardial infarction]. 833 1

Changes of ischemic myocardium following coronary occlusion, including active and passive functions, and adaptive changes of non-ischemic surviving myocardium have been summarized under the term "left ventricular remodeling" post myocardial infarction. An increase in left ventricular volume may be a consequence, and associated with an adverse prognosis. Although left ventricular dilatation may increase stroke volume and, thus, be compensatory at first, in about one-fifth of patients it ultimately results in progressive dysfunction and heart failure. Major determinants of this process are time, infarct size, infarct location, global left ventricular function assessed 4 days after infarction by radionuclide ejection fraction and right heart catheter (stroke volume), and morphology of the infarct-associated coronary artery. The surviving myocardium hypertrophies and may also dilate structurally. Depression of left ventricular ejection fraction chronically after the infarct is due to deterioration of wall motion of chamber segments initially classified normal by radionuclide analysis. Biochemical changes may also occur, including reduction of phosphocreatine, prolongation of time to peak Cai2+, and changes in myosin isoforms. Systemic or local humoral factors may be involved in these changes, however, clear evidence is still lacking. Perfusion of surviving myocardium may be altered under various conditions due to morphologic and functional changes of coronary vasculature. Successful prevention of heart failure and death by angiotensin converting enzyme inhibitors in asymptomatic patients with left ventricular dysfunction post-myocardial infarction has supported the pathophysiologic concepts of remodeling.
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PMID:Ventricular remodeling after myocardial infarction. Experimental and clinical studies. 835 28

The success of angiotensin-converting enzyme (ACE) inhibitors in reducing cardiovascular morbidity and mortality rates has led to a reexamination of the role of the renin-angiotensin system in pathophysiology. Ventricular dysfunction leading to congestive cardiac failure is associated with sequential activation of the sympathetic system and increases in plasma atrial natriuretic peptide; however, increases in plasma renin and aldosterone do not occur until very late. The renin-angiotensin system is now regarded as both a circulating and tissue hormonal system. All components of the renin-angiotensin system have been detected in the heart. ACE is localized in discrete areas of the heart, including the cardiac valves, coronary vessels, atria, and myocardium. After experimental myocardial infarction in the rat, although plasma renin and aldosterone levels are not increased, ACE in the myocardium is markedly increased. Treatment with ACE inhibitors suppresses cardiac ACE and is associated with hemodynamic improvement, reversal of the neurohumoral activation, prevention of ventricular dilatation, and remodeling and reduction in mortality rates. These results suggest that the beneficial effects of ACE inhibitors in treating congestive cardiac failure, preventing ventricular remodeling, and regressing left ventricular hypertrophy may involve not only reducing preload and afterload but also suppressing the local cardiac renin-angiotensin system.
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PMID:The cardiac renin-angiotensin system in heart failure. 836 49

A major consequence of chronic cardiac dysfunction is chronic overload of contractile myocardium. Various aetiologies, in reaction to this, may induce compensatory mechanisms consisting of excentric (dilatation) and concentric hypertrophy. Chronic left ventricular dysfunction is caused most frequently by myocardial infarction. Left ventricular dilatation and hypertrophy occurs in patients with extensive infarction. Dilatation may at first be compensatory, restoring stroke volume within 4 weeks of the infarct. However, as dilatation progresses, left ventricular ejection fraction and stroke volume deteriorate during exercise and at rest, and finally pulmonary capillary wedge pressure increases and patients become symptomatic 1.5-3 years after the infarct. Major determinants of progressive left ventricular dilatation and deterioration of haemodynamics are a depressed left ventricular ejection fraction, angiographically determined infarct size, stroke volume early (4 days) after myocardial infarction, infarct location (anterior/inferior) and the grade (TIMI) of perfusion of the infarct-associated coronary artery. Chronic loading and unloading may accelerate or decelerate this process. Efficiency and energy reserve (phosphocreatine) of the dilated ventricles is reduced. Further intrinsic changes in surviving myocardium include morphological and functional disturbance of coronary microcirculation.
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PMID:Cardiac dysfunction and development of heart failure. 837 Mar 60

Following a myocardial infarction the patient with a dilated heart is at greater risk for arrhythmias, congestive failure and sudden death. Studies of myocardial infarction in experimental animals have shown that, with infarcts involving up to 20% of the left ventricle, hypertrophy of surviving myocytes occurs and there are minimal hemodynamic changes. Infarctions greater than 20% induce little additional hypertrophy, and develop increased left ventricular filling pressures and cardiac dilatation. It has been suggested that inadequate hypertrophy of residual myocardium may be a reason for the progressive left ventricular dilatation which occurs after large myocardial infarcts. There are data in humans and animals suggesting that the mass of the left ventricle following a myocardial infarction correlates with improvement in systolic function. Studies from our laboratories have previously shown that 2-tetradecylglycidic acid, an inhibitor of carnitine palmitoyl transferase I, inhibits mitochondrial long-chain fatty acid oxidation and causes myocardial hypertrophy when given to rats by mouth for 7-28 days. We carried out studies to see whether induction of additional myocardial hypertrophy by means of feeding tetradecylglycidic acid might prevent pathologic dilation following a large (50%) infarct in rats. Treatment of control and infarcted rats with tetradecylglycidic acid for 10 days resulted in myocardial hypertrophy in both groups. The rats with myocardial infarction treated with tetradecylglycidic acid had an increase in peak developed left ventricular pressure during abrupt aortic occlusion and lower left ventricular end-diastolic volumes, when compared to untreated rats with myocardial infarction, while the stroke volume was maintained. Thus induction of myocardial hypertrophy with an inhibitor of long-chain fatty acid oxidation retarded the process of left ventricular dilatation and had beneficial effects on systolic function following a large myocardial infarction.
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PMID:A role of fatty acid oxidation in cardiac hypertrophy. 840 20

The mechanism of adverse effects of calcium channel blockade on cardiac performance and survival in patients with cardiac dysfunction after myocardial infarction is controversial. To test whether left ventricular dilatation and remodeling, as predictors of long-term survival and cardiac performance, are important, rats with healed infarcts received a vasodilating calcium channel blocker (anipamil) or placebo. After 8 weeks the mortality rate (total population n = 111) was 35% with calcium channel blockade and 4% with placebo in rats with infarction (p < 0.001). In survivors with large infarctions (44% +/- 12% of left ventricle, n = 9), calcium channel blockade did not aggravate left ventricular dysfunction and decreased chamber stiffness, but increased left ventricular volume (1.55 +/- 0.13 ml/kg, p = 0.03 vs placebo: 1.16 +/- 0.11 ml/kg; n = 11) (passive pressure-volume relationship) at persistently elevated volume/mass ratio. Thus this study shows for the first time that aggravation of left ventricular dilatation and remodeling is one important mechanism by which calcium channel blockade may reduce survival in the presence of ventricular dysfunction after myocardial infarction.
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PMID:Aggravation of left ventricular dilatation and reduction of survival by a calcium channel blocker in rats with chronic myocardial infarction. 848 May 73

Survival after myocardial infarction decreases with left ventricular dilatation, although dilatation at 4 weeks was found to be compensatory. To study this apparent discrepancy, prospective simultaneous volume and hemodynamic measurements at rest were extended in 39 patients with small and 37 with large myocardial infarctions from 4 days (range, 2-6 days) and 4 weeks (range, 3-5 weeks) to 6 months (range, 5-8 months) after infarction and were repeated during supine bicycle exercise at 50 W. In patients with small infarction, end-diastolic volume (mL/m2) decreased from 4 days to 6 months; ejection fraction (%), stroke volume (mL/m2), and end-systolic volume (mL/m2) remained unchanged. Stroke index rose during exercise at 4 weeks and 6 months. In patients after large infarction (n = 37), left ventricular end-systolic volume index (4 days, 38 +/- 3; 4 weeks, 47 +/- 3*; 6 months, 52 +/- 3*; *p < 0.05 versus 4 days) and end-diastolic volume indexes (4 days, 72 +/- 3; 4 weeks, 86 +/- 5*; 6 months, 92 +/- 5*; *p < 0.05 versus 4 days, +p < 0.05 versus 4 weeks) increased at constant wedge pressure. Stroke index remained restored beyond 4 weeks after infarction (4 days, 35 +/- 2; 4 weeks, 42 +/- 2*; 6 months, 42 +/- 2*; p < 0.05 versus 4 days) and rose during exercise at 4 weeks (rest, 45 +/- 2; exercise, 55 +/- 3; p < 0.05) but not at 6 months (rest, 42 +/- 3; exercise, 45 +/- 3; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adaptation to cardiac dysfunction after myocardial infarction. 848 38

Collagen which is present in the myocardium in relatively small amounts is the most abundant structural protein of the connective tissue network. Its structural organization consists of a complex weave of collagen fibers that surrounds and interconnects myocytes, groups of myocytes, muscle fibers and muscle bundles. The conformation of interstitial fibrillar collagen makes it highly resistant to degradation by all proteinases other than specific collagenases. In hearts with myocardial damage secondary to myocardial infarction, chronic ischemia, inflammation, or cardiomyopathy, a complex sequence of compensatory events occur that eventually result in an adverse left ventricular remodeling. This continual state of remodeling is characterized by persistent collagenase activity, fibrillar collagen degradation, and progressive myocyte loss. The net effect is a shift in the balance between collagen synthesis and degradation which leads to an inadequate fibrillar collagen matrix, progressive ventricular dilatation and sphericalization with wall thinning and eventual congestive heart failure.
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PMID:Ventricular remodeling in heart failure: the role of myocardial collagen. 854 Apr 1

The chronic changes of the end-systolic pressure-volume relationship (ESPVR) after regional myocardial infarction were evaluated in a sheep model. Pressure-volume area (PVA) obtained from the pressure-volume diagram and left ventricular oxygen consumption (LVO2) were studied. The regional myocardial infarction was created by ligating distal branches of the left coronary artery. ESPVR was obtained using a conductance catheter during transient inferior vena cava occlusion. Measurements were performed at baseline (n = 13), 1 hour (n = 8), 3 months (n = 9), and 6 months (n = 4) after infarction. Ees, the slope of the ESPVR did not change at 1 hour after infarction and remained the same at 3-month and 6-month measurements (baseline 2.26 +/- 1.24 mmHg/mL, 1 hour 2.71 +/- 1.06, 3 months 3.46 +/- 1.51, 6 months 2.45 +/- 0.64, NS). Because of the ventricular dilatation, which was demonstrated as an increase in changes of end-systolic volume (Ves) correlating with the time course after infarction (y = -3.21 + 0.12x, r = 0.454, p < 0.05), V0, the volume intercept of the ESPVR increased at 1 hour after the infarction, and showed a tendency to increase at 3 months and 6 months after the infarction (baseline -18.0 +/- 22.5 mL; 1 hour -0.9 +/- 11.6; 3 months 5.4 +/- 10.9, 6 months 9.2 +/- 23.1, baseline vs 3 months p < 0.05, baseline vs 6 months p < 0.05). PVA and LVO2 were unchanged over time after infarction (PVA: baseline 2097 +/- 1526 mmHg/mL per 100 g-1; 1 hour 1771 +/- 699; 3 months 2483 +/- 1086; 6 months 1,608 +/- 1,010, NS), (LVO2: baseline 40.6 +/- 13.1 x 10(-3) mL/100 g-1 per beat-1; 1 hour 42.9 +/- 9.7; 3 months 35.0 +/- 8.6; 6 months 31.2 +/- 18.1, NS). Chronic regional infarction in the sheep model did not affect Ees over 6 months, but significantly increased V0 after the increase in the acute phase. PVA and LVO2 were not affected by this regional infarction either acutely or over 6 months.
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PMID:Chronic changes of end-systolic pressure-volume relationship after regional myocardial infarction. 857 24

The use of ACE-inhibitors in heart failure has been established over the past years. Their use is of uncertain value in the early phases of myocardial infarction, where they are supposed to prevent left ventricular dilatation. More recent studies (ISIS-4, GISSI-3) have tested early treatment by ACE-inhibitors in the acute phase of myocardial infarction. On one hand, it was possible to disprove reservations about risks (hypotension)n in a large cohort; on the other hand, a further reduction of mortality in hospitalized patients by 7% has been shown, corresponding to five patient lives saved for 1000 treated patients. Thus, after institution of the customary therapy of myocardial infarction (inhibitor of platelet aggregation, thrombolysis, beta-blocker) and after exclusion of specific contraindications (hypotension < 100 mmHg, renal failure) ACE-inhibitors could be administered in the acute phase of myocardial infarction. An analysis of the results from these large trials will show whether ACE-inhibitors may benefit groups of patients at particular risks (Killip > 1, age > 70 years, preceding renal failure) noticeably. ACE-inhibitors remain the treatment of choice in patients with developing left ventricular failure.
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PMID:[ACE-inhibitors in acute heart infarct]. 866 93


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