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PubMed1991

[Echocardiography: a quantitative evaluation method of ventricular remodeling].

Left ventricular remodeling consists of changes in size and geometry of the left ventricular cavity associated with changes in wall thickness. These changes occur in different conditions such as during growth, pressure or volume overload or after myocardial infarction. Echocardiography in M or two dimensional modes provides a means of evaluating global and regional left ventricular function and of measuring variations of wall thickness during the cardiac cycle. Using mathematical models in the parasternal (surface-length method) or apical views (Simpson's method) of the left ventricle, the end diastolic and end systolic volumes and ejection fraction can be calculated with reasonable accuracy, so enabling detection of spontaneous or therapeutically-induced variations of clinical significance. The extent of the akinetic or dyskinetic myocardium can be compared with the diastolic perimeter and expressed as a percentage value. This parameter is one of the quantitative values for expressing "expansion" of the necrosed segment and the changes occurring in the non-infarcted areas. M-mode echocardiography more than the two dimensional mode enables measurement of wall thickness and calculation of myocardial mass, providing the clinician with an assessment of myocardial hypertrophy and its relation to left ventricular chamber size (wall thickness/LV radius ratio). Of the different available methods of cardiac imaging, echocardiography is the most widely used because it is non-invasive and can be used repetitively to document the progressive changes in size and wall thickness of the left ventricle, known as "remodeling".

Cardiomegaly↗

PubMed1992

Ventricular remodeling following myocardial infarction.

Ventricular remodeling denotes structural changes that occur in ventricular chamber size, wall thickness, and composition following myocardial damage. Following acute coronary occlusion, there are various factors to consider at different times that may contribute to subsequent ventricular dilation. Early infarct expansion and later healing may be accompanied by compensatory hypertrophy in the noninfarcted region and progressive global dilation, that may progress long term, the major stimulus being increased wall stress. The 2 major factors influencing ventricular remodeling following myocardial infarction are infarct artery patency and the ventricular loading conditions. Thrombolytic therapy may produce coronary reperfusion and limit infarct size. Patency of the infarct-related artery may also provide later benefits for ventricular remodeling. Following infarct evolution, pharmacologic intervention provides the potential to minimize the sequelae of infarct expansion and ventricular dilation. Clinical studies indicate that treatment of symptomless left ventricular dysfunction with angiotensin-converting enzyme inhibition at greater than or equal to 1 week following myocardial infarction may prevent further ventricular dilation and reduce the probability of progression to heart failure. Earlier intervention, at 24-48 hours following Q-wave myocardial infarction, is also practicable and effective. Even earlier intervention, in combination with or immediately following thrombolysis, is being assessed in other studies. The timing of treatment is of considerable importance because blockade of compensatory mechanisms activated at the time of infarction may not be desirable immediately, even though these mechanisms may be deleterious later. The results of large-scale mortality studies are awaited to indicate the benefit of this type of treatment in terms of heart failure prevention and survival long term.

Humans↗

PubMed1992

[Left ventricular remodeling after myocardial infarction].

Left ventricular remodeling describes a number of geometric and structural changes that the left ventricle undergoes after myocardial infarction. Briefly, it comprises expansion of the infarct and dilatation of the healthy left ventricular segments. Its severity is related to the infarct size. These changes in ventricular geometry, in particular the dilatation, influence the long-term incidence of cardiac failure, the main secondary complication of myocardial infarction. Up to now, therapeutic interventions have been oriented to reducing the infarct size with the aim of avoiding or delaying the occurrence of left ventricular dysfunction. Nowadays, it seems possible to influence the natural process of post-infarction. Left ventricular remodeling independently of efforts to reduce infarct size. There is evidence that this process may be limited pharmacologically with angiotensin converting enzyme inhibitors. In animal studies, these agents limit remodeling and improve survival after myocardial infarction, but for the moment, despite confirmed benefits on left ventricular modeling, it is not possible to extrapolate these results in terms of clinical mortality.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1991

Effects of milrinone on left ventricular remodeling after acute myocardial infarction.

BACKGROUND: Left ventricular remodeling after an acute myocardial infarction may result in progressive left ventricular dilation that may be associated with increased mortality. We studied the effects of the phosphodiesterase inhibitor milrinone on left ventricular remodeling after acute myocardial infarction. METHODS AND RESULTS: Rats (n = 90) were randomized to undergo either left coronary artery ligation or sham operation. Three weeks after surgery, rats received either no treatment or milrinone, which was continued until 2 days before the rats were killed. Ninety days after the initial surgery, hemodynamic measurements were made before and after volume loading. The rats were killed, the hearts were removed, and passive pressure-volume curves were obtained. The hearts were fixed at a constant pressure and analyzed morphometrically. Compared with untreated infarcted rats, milrinone-treated infarcted rats had a lower left ventricular end-diastolic pressure (1.7 +/- 0.4 versus 4.3 +/- 1.4 mm Hg, p less than 0.05), a lower left ventricular volume (1.25 +/- 0.20 versus 2.37 +/- 0.30 ml/kg, p less than 0.001) and a lower left ventricular wall stress index (1.3 +/- 0.2 versus 1.7 +/- 0.1, p less than 0.05). Left ventricular chamber stiffness was higher in milrinone-treated infarcted rats than in untreated infarcted rats. Milrinone had no cardiac effect on uninfarcted animals. CONCLUSION: Chronic milrinone therapy after acute myocardial infarction improves cardiac hemodynamic indexes and attenuates progressive left ventricular dilation.

Animals↗

PubMed1992

Medical repair of hypertensive left ventricular remodeling.

Hypertensive left ventricular (LV) hypertrophy leads to myocytic hypertrophy, interstitial fibrosis, and structural alterations of the coronary microcirculation. This structural remodeling of the myocardium results in an impairment of diastolic function of the left ventricle and of coronary flow reserve despite normal epicardial arteries. Consequently, an antihypertensive treatment should aim at (a) reversing myocytic hypertrophy, (b) regression of myocardial fibrosis, and (c) improvement of coronary flow reserve apart from blood pressure lowering. In recent years many clinical studies have shown that regression of hypertensive hypertrophy can be induced by long-term treatment with angiotensin-converting enzyme (ACE) inhibitors, calcium-channel blockers, beta-receptor blockers, and antisympathonic drugs. However, vasodilators and diuretics, which stimulate adrenoceptor activity and increase angiotensin II levels, were found to be less effective in reversing LV hypertrophy. The trophic influence of catecholamines and angiotensin II on the myocardium counteracts the effect of systolic wall stress reduction due to blood pressure lowering. In respect of reversal of interstitial fibrosis, ACE inhibitors seem to be effective because the growth of fibroblasts was found to be stimulated by angiotensin II. Recently, clinical studies have confirmed previous experimental data that an improvement of the impaired coronary vasodilator reserve can be realized by long-term antihypertensive therapy. An antihypertensive treatment strategy which fully restores myocardial structure and completely repairs coronary microcirculation has to be considered as a causative treatment of hypertensive heart disease.

Adrenergic beta-Antagonists↗

PubMed1992

Left ventricular remodeling after myocardial infarction: does the cardiac renin-angiotensin system play a role?

Possible cardioprotective effects are one of the most intriguing aspects of the expanding spectrum of clinical indications for the use of converting-enzyme inhibitors. Among them, the prevention of postinfarction ventricular remodeling--a deleterious process leading to eccentric cardiac hypertrophy and, eventually, to congestive heart failure--has attracted particular interest and attention. This communication examines the possible role of the endogenous cardiac renin-angiotensin system in the pathophysiology of ventricular remodeling. Although much of the evidence is indirect, there are several lines of investigation that strongly support the causative participation of the cardiac renin-angiotensin system in ventricular remodeling.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1992

Effects of captopril treatment on left ventricular remodeling and function after anterior myocardial infarction: comparison with digitalis.

The effects of captopril and digoxin treatment on left ventricular remodeling and function after anterior myocardial infarction were evaluated in a randomized unblinded trial. Fifty-two patients with a first transmural anterior myocardial infarction and a radionuclide left ventricular ejection fraction less than 40% were randomly assigned to treatment with captopril (Group A) or digoxin (Group B). The two groups had similar baseline hemodynamic, coronary angiographic, echocardiographic and radionuclide angiographic variables. Among the 40 patients (20 in each group) who were followed up for 1 year, echocardiographic end-diastolic and end-systolic volumes were unmodified in Group A and global wall motion index was improved (p less than 0.01); in Group B, end-diastolic and end-systolic volumes increased (p less than 0.001 for both) and global wall motion index was unchanged. Rest radionuclide ejection fraction increased significantly in both groups (p less than 0.001, Group A; p less than 0.005, Group B). A comparison of the changes in the considered variables between the two groups after 1 year of treatment showed a difference in end-diastolic (p less than 0.005) end-systolic volumes (p less than 0.001) and global wall motion index (p less than 0.005) without differences in radionuclide ejection fraction, which improved to a similar degree in both groups. The results of this study suggest that captopril therapy, started 7 to 10 days after symptom onset in patients with anterior myocardial infarction and an ejection fraction less than 40%, improves both left ventricular remodeling and function and prevents left ventricular enlargement and in these patients performs better than digitalis.

Captopril↗

PubMed1990

Severe myocardial dysfunction induced by ventricular remodeling in aging rat hearts.

To determine if aging engenders alterations in the functional properties of the myocardium and ventricular remodeling, the hemodynamic performance and structural characteristics of the left ventricle of male Fischer 344 rats at 4, 12, 20, and 29 mo of age were studied by quantitative physiology and morphology. In vivo assessment of cardiac pump function showed no change up to 20 mo, whereas left ventricular end-diastolic pressure was increased at 29 mo. Moreover, peak rates of pressure rise and decay, stroke volume, ejection fraction, and cardiac output were depressed at the later age interval, demonstrating the presence of ventricular failure at this time. The measurements of chamber size and wall thickness showed that ventricular end-diastolic and end-systolic volumes progressively increased with age with the greatest change occurring at 20-29 mo. Aging was also accompanied by a marked augmentation in the volume fraction of fibrotic areas in the ventricular myocardium that was due to an increase in their number and cross-sectional area with time. These architectural rearrangements, in combination with the abnormalities in ventricular function, resulted in an elevation in the volume of wall stress throughout the cardiac cycle. Wall stress increased by 64, 44, and 50% from 4 to 12, 12 to 20, and 20 to 29 mo of age. In conclusion, aging leads to a continuous rise in wall stress that is not normalized by ventricular remodeling. These two independent processes appear to be responsible for the onset of heart failure in the senescent rat.

Aging↗

PubMed1991

[Left ventricular remodeling in hypertension. Physiopathology].

The usual concept of ventricular hypertrophy is simple and logical: increased systolic wall stress induces a hypertrophic reaction which is 1) symmetrical affecting all ventricular walls harmoniously, 2) concentric, developing at the expense of cavity size, increasing the thickness to radius ratio, and, 3) appropriate allowing normalisation of wall stress. This hypertrophy appears initially to be useful as it contributes to the maintenance of systolic function in the face of increasing load. However, it is accompanied by abnormalities of ventricular filling, of coronary circulation and myocardial excitability which may have undesirable consequences on the prognosis. In fact this simplistic and didactic view is inadequate for describing the complexity of left ventricular remodeling in hypertension. This is apparent at three levels at least: the stimuli responsible; if increased wall stress is a necessary and sometimes in itself enough to induce hypertrophy, other mechanisms may effect the degree and nature of this reaction; the protein, cellular and tissular expression; this is particularly true with respect to the connective (collagen) tissue which seems to develop in response to distinct stimuli and which could have an important influence on the functional properties of the myocardium; the morphological expression; this is the only parameter which can be analysed directly by the clinician by echocardiography. This investigation enables assessment of the frequency of eccentric and asymmetric forms of hypertrophy, the significance of which remains unclear.

Cardiomegaly↗

PubMed1991

[Left ventricular remodeling and ischemic heart diseases. Therapeutic possibilities].

Left ventricular modeling after myocardial infarction may be modified in three ways: firstly, by limiting the infarct size; secondly, by administering ACE inhibitors: these drugs limit infarct expansion and ventricular dilatation. They reduce the prevalence of secondary left ventricular failure and, in the animal, improve the prognosis. Glyceryl trinitrate also appears to be effective. The third therapeutic option is maintaining the patency of the artery responsible for the infarction, which has a beneficial effect on ventricular remodeling. The respective therapeutic indications of these three options are still a matter of discussion.

Adrenergic beta-Antagonists↗

PubMed1992

Ventricular remodeling following myocardial infarction: a description of the pathologic process, current investigation, and suggested therapy.

The pathophysiologic process of ventricular remodeling after AMI involves an alteration in myocardial cell contraction. The stretching and redistribution of myocardial cells in the ischemic area promote dyssynergic contraction and an overall reduction in ventricular function. Expansion of the infarcted area and volume-overload hypertrophy of the uninfarcted area remodel the shape of the ventricle. Ventricular enlargement and dilation are associated with early mortality and morbidity. This has prompted further study to identify measures that can attenuate the process. Limited investigation on human subjects suggests that ACE inhibition reduces ventricular wall stress and preserves ventricular shape and function. A multicenter trial, SAVE, is under way to study the effects of long-term captopril therapy for patients suffering from AMI. This study and future investigations will focus on inhibition of ventricular remodeling following AMI in the hope of reducing symptomatic CHF and mortality.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1991

Cellular basis of ventricular remodeling after myocardial infarction.

To determine whether acute left ventricular failure associated with myocardial infarction leads to architectural changes in the spared nonischemic portion of the ventricular wall, large infarcts were produced in rats, and the animals were sacrificed 2 days after surgery. Left ventricular end-diastolic pressure was increased, whereas left ventricular dP/dt and systolic pressure were decreased, indicating the presence of severe ventricular dysfunction. Absolute infarct size, determined by measuring the fraction of myocyte nuclei lost from the left ventricular free wall, averaged 63%. Transverse midchamber diameter increased by 20%, and wall thickness diminished by 33%. The number of mural myocytes in this spared region of the left ventricular free wall decreased by 36% and the capillary profiles by 40%. Thus, side-to-side slippage of myocytes in the myocardium occurs acutely in association with ventricular dilation after a large myocardial infarction. In order to analyze the chronic consequences of myocardial infarction on ventricular remodeling, a second group of experiments was performed in which the left coronary artery was ligated and the functional and structural properties of the heart were examined 1 month later. In infarcts affecting an average 38% of the free wall of the left ventricle (small infarcts), reactive hypertrophy in the spared myocardium resulted in a complete reconstitution of functioning tissue. However, left ventricular end-diastolic pressure was increased, left ventricular dP/dt was decreased, and diastolic wall stress was increased 2.4-fold. After infarctions resulting in a 60% loss of mass (large infarcts), a 10% deficit was present in the recovery of viable myocardium. Functionally, ventricular performance was markedly depressed, and diastolic wall stress was increased 9-fold. The alterations in loading of the spared myocardium were due to an increase in chamber volume and a decrease in the myocardial mass/chamber volume ratio that affected both infarct groups. Thus, decompensated eccentric ventricular hypertrophy develops chronically after infarction and growth processes in myocytes are inadequate for normalization of wall stress when myocyte loss involves nearly 40% or more of the cells of the left ventricular free wall. The persistence of elevated myocardial and cellular loads may sustain the progression of the disease state toward end-stage congestive heart failure.

Animals↗

PubMed1991

[Left ventricular remodeling and hypertension. Course with antihypertensive therapy].

Changes in left ventricular remodeling due to antihypertensive therapy have been demonstrated in experimental animal studies although no quantitative relationship has been shown between correction of blood pressure and regression of myocardial mass. As regards the qualitative aspects of regression, only the ACE inhibitors have been shown to prevent the development and induce regression of the excess collagen content of the myocardium submitted to chronic pressure overload. The problems posed by remodeling in clinical practice are more complex: should regression of myocardial mass itself be the therapeutic objective in the absence of a practical method of analysing the interstitial factor of hypertensive disease or should we concentrate on the satellite problems of hypertrophy which are correction of ischemia, left ventricular filling abnormalities and arrhythmias. For each of these clinical problems, the benefits attributed to changes in remodeling, though probable, are to a large degree hypothetical. The benefits offered by these drugs which reduce ventricular hypertrophy are, however, considerable.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1991

[Ventricular "remodeling" after myocardial infarction].

Cardiac failure is the principal medium-term complication of myocardial infarction. Changes in left ventricular geometry are observed after infarction, called ventricular remodeling, which, though compensatory initially, cause ventricular failure in the long-term. Experimental and clinical studies suggest that early treatment by coronary recanalisation, trinitrin and angiotensin converting enzyme inhibitors may prevent or limit the expansion and left ventricular dilatation after infarction, so improving ventricular function, and, at least in the animal, reduce mortality. Large scale trials with converting enzyme inhibitors are currently under way to determine the effects of this new therapeutic option. It would seem possible at present, independently of any reduction in the size of the infarction, to reduce or delay left ventricular dysfunction by interfering with the natural process of dilatation and ventricular modeling after infarction.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1990

Effects of late administration of tissue-type plasminogen activator on left ventricular remodeling and function after myocardial infarction.

To evaluate the effects of late thrombolysis on left ventricular volume and function in acute myocardial infarction, two-dimensional echocardiography and radionuclide angiography were performed before discharge and after 1 year of follow-up study in 34 patients with acute anterior myocardial infarction. Of these, 10 admitted to the coronary care unit within 4 h from the onset of symptoms were treated with recombinant tissue-type plasminogen activator (rt-PA) (Group A) and 24 admitted between 4 and 8 h after onset were randomly assigned to receive either rt-PA (Group B, n = 12) or conventional therapy (Group C, n = 12). Seven to 10 days after admission, all patients underwent cardiac catheterization and coronary angiography. Patency of the infarct-related vessel was 70% in Group A, 66% in Group B and 33% in Group C and the average Thrombolysis in Myocardial Infarction (TIMI) coronary perfusion grade was 1.9 +/- 0.8 for Group A, 1.6 +/- 1.0 for Group B and 0.84 +/- 0.95 for Group C (Group A versus Group C p less than 0.01; Group B versus Group C p less than 0.05). At predischarge evaluation, mean left ventricular end-systolic and end-diastolic volumes were higher in Group C than in Group B (p less than 0.001 and 0.05, respectively) and Group A (p less than 0.005 for both); mean left ventricular ejection fraction at rest was lower in Group C than in Group B and Group A (p less than 0.05 for both). At 1 year follow-up study, end-systolic and end-diastolic volumes remained higher in Group C than in Group B (p less than 0.05 for both) and Group A (p less than 0.005 for end-systolic volume and p less than 0.001 for end-diastolic volume); ejection fraction at rest was lower in Group C than in Groups A and B (p less than 0.05 for both); during exercise, it increased more in Group A than in Group C (p less than 0.01). Comparison of data obtained before discharge and at the 1 year follow-up study revealed a significant differences in end-systolic volume (p less than 0.05) in Group C patients and in end-diastolic volume in patients in Groups B (p less than 0.05) and C (p less than 0.001). The beneficial effect of late thrombolysis with rt-PA may be related to a reduction in myocardial expansion and thus to a favorable influence on postinfarction left ventricular remodeling.

Coronary Vessels↗

PubMed1991

Sequential echocardiographic-Doppler assessment of left ventricular remodelling and mitral regurgitation during evolving experimental heart failure.

STUDY OBJECTIVE: The aim was to study the nature, magnitude, and time course of left ventricular structural adaptations to evolving heart failure. DESIGN: 17 male mongrel dogs, weight 24.9(SD 3.7) kg, underwent rapid ventricular pacing (250 beats.min-1) until severe heart failure developed. Two dimensional echocardiographic and Doppler studies were performed at control, then weekly to severe heart failure. Haemodynamic measurements were made at control and severe heart failure. All studies were performed with the animals conscious during temporary sinus rhythm. MEASUREMENTS AND MAIN RESULTS: Left ventricular diastolic volume gradually increased and the left ventricle assumed a more globular shape associated with significant wall thinning. Both the change in diastolic volume after one week of pacing and at the time of severe heart failure correlated with the time to peak heart failure. Mitral regurgitation was mild after one week of pacing, became moderate in most animals at severe heart failure, and lagged temporarily behind the increase in cardiac dimensions. The percentage increase in mitral annular size was significantly less than the increase in left ventricular cross sectional area. CONCLUSIONS: In pacing induced heart failure (1) marked left ventricular remodelling occurs, (2) the extent of left ventricular dilatation, both early and late, correlates directly with the time required for the development of severe heart failure, (3) mitral regurgitation is an epiphenomenon and is most likely to be caused by the increase in left ventricular cross sectional area.

Animals↗

PubMed1992

Effect of long-term captopril therapy on left ventricular remodeling and function during healing of canine myocardial infarction.

To determine whether the long-term reduction of preload and afterload by captopril during healing after acute anterior myocardial infarction might attenuate left ventricular remodeling and improve function, 30 chronically instrumented dogs with infarction produced by left anterior descending coronary artery ligation were randomized 2 days later to oral therapy with placebo (n = 15) or captopril, 50 mg twice daily (n = 15), for 6 weeks. Serial hemodynamic as well as topographic and functional variables (two-dimensional echocardiography) were measured over 6 weeks. Scar topography (planimetry), occluded bed size (coronary arteriography) and collagen (hydroxyproline) content were measured at 6 weeks. Between 2 days and 6 weeks, captopril decreased (p less than 0.001) mean arterial pressure and mean left atrial pressure more than did placebo, but it did not influence heart rate. Infarct scar mass, transmurality and collagen content at 6 weeks were similar in the two groups but scars showed less (p less than 0.001) thinning and expansion with captopril than with placebo. Echocardiograms showed similar infarct expansion and thinning in the two groups at 2 days but less aneurysm with captopril at 6 weeks. Between 2 days and 6 weeks, expansion index (infarct-/noninfarct-containing segment length) decreased (p less than 0.001) with captopril but increased (p less than 0.001) with placebo. Also, thinning ratio (infarct/normal wall thickness) decreased (p less than 0.001) with placebo but did not change (p = NS) with captopril. By 6 weeks, left ventricular asynergy and volumes showed a greater decrease (p less than 0.01) and global ejection fraction a greater increase (p less than 0.05) with captopril.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Heterogeneity of ventricular remodeling after acute myocardial infarction in rats.

To determine the effects of acute myocardial infarction on the extent and distribution of systolic and diastolic wall stress on the surviving myocardium, coronary artery occlusion was produced in rats, and the animals were killed 1 wk later. After hemodynamic measurements in vivo, the characteristics of cardiac anatomy at end diastole and peak systole were mimicked in vitro by fixing hearts under diastolic conditions or barium-induced contracture. In the presence of infarcts inducing a 48% loss of myocytes, left ventricular failure was documented by increases in left ventricular minimal and end-diastolic pressures and decreases in peak systolic pressure and positive and negative rates of pressure change with time. End-diastolic and end-systolic volumes increased, whereas stroke volume and cardiac output diminished. Ventricular remodeling in diastole consisted of an increase in the longitudinal axis while both longitudinal and transverse mid-chamber diameters were augmented after systolic contraction. Left ventricular chamber volume enlarged by 44% through a 20% augmentation in the longitudinal diameter and increases in the transverse luminal diameter of 13, 21, 32, and 37% in four consecutive sites from the equatorial region to the apex. As a consequence of infarction, systolic thickening of the spared myocardium of the free wall was reduced progressively from the base to the apex. In the interventricular septum of the infarcted heart, systole thickening occurred mostly in the equatorial region and was reduced at the basal and apical portions. The interaction of hemodynamic impairment with the architectural rearrangements of the wall and chamber provoked a 1.9-fold increase in overall stress on the spared myocardium. However, diastolic stress was augmented by 6.8-fold, markedly exceeding the 1.1-fold increase in systolic stress. Thus large infarcts of the rat left ventricle due to left main coronary occlusion lead to a change in shape of the heart from ellipsoidal to cylindrical. The elevation in overall stress may condition the unfavorable long-term outcome of the infarcted heart.

Animals↗