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PubMed1987

Left ventricular sensitivity to beta-adrenoceptor-stimulating drugs in patients with ischemic heart disease and varying degrees of ventricular dysfunction.

The left ventricular sensitivity to sympathomimetic amines was assessed in 47 patients with ischemic heart disease and varying degrees of left ventricular dysfunction. Patients were divided into 3 subgroups according to their basal ejection fraction (less than or equal to 35%, between 36 and 54%, and greater than or equal to 55%). After injection of a bolus of isoproterenol (2 micrograms), the isovolumic indexes of inotropic state increased significantly less in patients with an ejection fraction less than or equal to 35% than in other patients, but the heart rate changes and the acceleration in the rate of isovolumic pressure fall were comparable in all subgroups. The dose-response curves to cumulative doses of xamoterol, a beta 1-adrenoceptor partial agonist, confirmed that the magnitude of the inotropic response was reduced during beta 1-stimulation in patients with an ejection fraction less than or equal to 35% when compared with patients with a greater ejection fraction. However, the dose of xamoterol necessary to produce 50% of the maximal inotropic response was not increased in patients with an ejection fraction less than or equal to 35% (range, 1.5-5.2 micrograms/kg; median 2.5 vs. median values of 2.3 and 3.3 micrograms/kg in the other subgroups; NS), and there was no shift to the right of the dose-response curve. It is concluded that in moderate ischemic heart failure, the magnitude of the inotropic response to isoproterenol or xamoterol is reduced. The absence of shift to the right of the dose-response curve to a beta 1-partial agonist suggests that this alteration in myocardial performance is not primarily caused by a decrease in beta-adrenoceptor responsiveness.

Aged↗

PubMed1996

Natriuretic peptides and cyclic guanosine 3',5'-monophosphate in asymptomatic and symptomatic left ventricular dysfunction.

BACKGROUND: Screening for patients with asymptomatic left ventricular dysfunction is of considerable importance because they may benefit from early treatment with angiotensin converting enzyme inhibitors. It has been suggested that atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and cyclic guanosine 3',5'-monophosphate (cGMP) might be useful markers for screening. OBJECTIVE: To compare directly the power of the three immunoreactive forms of ANP (CT-ANP, beta-ANP, NT-ANP) and BNP and cGMP to detect asymptomatic left ventricular dysfunction. METHODS AND RESULTS: Radionuclide ventriculography was used to study left ventricular ejection fraction in 37 patients with asymptomatic left ventricular dysfunction, 32 patients with mild to moderate congestive heart failure, and 38 controls. CT-ANP, NT-ANP, beta-ANP, BNP, and cGMP were measured at rest and 3 minutes after exercise. Plasma BNP was the most sensitive marker for patients with asymptomatic left ventricular dysfunction but it reached only a sensitivity of 58% and a specificity of 76% at rest and a sensitivity of 65% and a specificity of 84% after exercise. Combined measurements of all natriuretic peptides and cGMP did not improve the power to detect asymptomatic left ventricular function above that of a single BNP measurement. CONCLUSIONS: Although natriuretic peptides and cGMP measured at rest and three minutes after ergometry may be useful for monitoring left ventricular dysfunction they are unlikely to be suitable for more general routine screening for completely asymptomatic left ventricular dysfunction.

Adult↗

PubMed1999

Disruption of the relationship between renin and atrial natriuretic peptide early in the course of ventricular dysfunction.

BACKGROUND: Plasma renin activity is normal in left ventricular dysfunction in the absence of diuretic therapy. In health there is a reciprocal relationship between renin and atrial natriuretic peptide (ANP) but a positive correlation in advanced heart failure. The relationship between renin and ANP in mild left ventricular dysfunction is unknown. METHODS AND RESULTS: Patients with left ventricular dysfunction (n = 35, 18 without diuretic therapy) were compared to 20 age-matched healthy subjects. Plasma concentrations of active renin (PARC), ANP and norepinephrine were measured after 20 min rest and 45 min after an infusion of normal saline (10 ml/kg body wt.). Basal plasma ANP was increased in patients with left ventricular dysfunction compared to healthy subjects, whether or not they were receiving diuretics. PARC was similar in healthy controls and patients untreated with diuretics but was increased in diuretic treated patients. After saline loading in healthy subjects PARC fell while ANP rose. Patients with left ventricular dysfunction had a smaller decline in PARC, that did not achieve statistical significance, but had a greater increase in plasma ANP compared to healthy subjects (P<0.05). The close reciprocal relationship between PARC and ANP observed in healthy subjects before and after saline loading (r = 0.8, P<0.001 and r = 0.6, P<0.01) was weakened in those not receiving diuretics (r = 0.4, P<0.05 and r = 0.24, ns) and lost in those receiving diuretics (r = 0.1 and r = 0.08). CONCLUSIONS: Patients with left ventricular dysfunction have a disturbance of the normal reciprocal relationship between PARC and ANP which antedates diuretic treatment. This should be taken into account when interpreting plasma neuroendocrine measurements in patients with ventricular dysfunction.

Atrial Natriuretic Factor↗

PubMed1987

Circulatory support for right ventricular dysfunction.

New modes of circulatory support for right ventricular dysfunction have recently been described. The present study compared the effectiveness of pulmonary artery balloon counterpulsation with a right ventricular assist device for support of surgically induced right ventricular dysfunction. Right ventricular hypertrophy was created in 16 neonatal lambs by pulmonary artery banding. Right ventricular dysfunction was produced in all animals by performing a right ventriculotomy and maintaining the pulmonary artery band. Four unassisted animals developed severe acute right heart failure and died. Six sheep had pulmonary artery balloon counterpulsation with a Dacron graft anastomosed to the proximal pulmonary artery as a reservoir for a 40 ml intra-aortic balloon after the onset of heart failure. The remaining six sheep had a pneumatically activated ventricular assist device inserted between the proximal pulmonary artery and the right ventricular apex. Periods of circulatory support with the balloon pump and the assist device on and off were compared. Decreases in right atrial pressure were observed with both balloon counterpulsation and right ventricular assistance: 14 +/- 1 to 11 +/- 1 mm Hg, p less than 0.0001, versus 19 +/- 2 to 12 +/- 2 mm Hg, p less than 0.0002, respectively. Cardiac output increased with both balloon counterpulsation and ventricular assistance: 1.45 +/- 0.16 to 2.03 +/- 0.13 L/min, p less than 0.001, versus 0.72 +/- 0.15 to 2.24 +/- 0.23 L/min, p less than 0.0002, respectively. Aortic systolic pressure increased in both support groups: 78 +/- 7 to 99 +/- 6 mm Hg, p less than 0.0004, versus 53 +/- 9 to 85 +/- 9 mm Hg, p less than 0.0001, respectively. Ventricular assistance produced greater changes in the right atrial pressure (39% +/- 6% versus 17% +/- 3%, p less than 0.01), cardiac output (153% +/- 39% versus 54% +/- 11%, p less than 0.05), and aortic systolic pressure (85% +/- 13% versus 39% +/- 9%, p less than 0.01). The insertion of a right ventricular assist device caused a significant increment in right ventricular dysfunction. These data, obtained with the devices in place but not operating, showed significantly increased right atrial and right ventricular end-diastolic pressures and approximately 50% less cardiac output than with the pulmonary artery balloon counterpulsation system. The results demonstrate that both modes of circulatory support were effective in reversing surgically induced right ventricular failure.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1995

A functional role for endogenous atrial natriuretic peptide in a canine model of early left ventricular dysfunction.

Asymptomatic or early left ventricular dysfunction in humans is characterized by increases in circulating atrial natriuretic peptide (ANP) without activation of the renin-angiotensin-aldosterone system (RAAS). We previously reported a canine model of early left ventricular dysfunction (ELVD) produced by rapid ventricular pacing and characterized by an identical neurohumoral profile and maintenance of the natriuretic response to volume expansion (VE). To test the hypothesis that elevated endogenous ANP suppresses the RAAS and maintains sodium excretion in ELVD, we assessed the effects of antagonism of ANP on cardiorenal and neurohumoral function in ELVD. Chronic ANP suppression was produced by bilateral atrial appendectomies before the production of ELVD by rapid ventricular pacing (ELVD-APPX, n = 5). This group was compared with a separate group with ELVD and intact atrial appendages (ELVD-INTACT, n = 8). ELVD-APPX was characterized by lower circulating ANP (50 +/- 11 vs. 158 +/- 37 pg/ml, P < 0.05), activation of plasma renin activity (PRA) (9.4 +/- 2.4 vs. 0.6 +/- 0.4 ng/ml per h, P < 0.05) and aldosterone (36.4 +/- 12.5 vs. 2.5 +/- 0.0 ng/dl, P < 0.05) when compared to ELVD-INTACT. In comparison to the ELVD-INTACT group, sodium excretion was decreased before and during VE in the ELVD-APPX group. Acute ANP antagonism was produced by administration of the particulate guanylate cyclase coupled natriuretic peptide receptor antagonist, HS-142-1, to seven conscious dogs with ELVD and intact atrial appendages (ELVD-INTACT). HS-142-1 decreased plasma concentrations and renal generation of the ANP second messenger, cGMP, and was associated with activation of PRA and sodium retention with enhanced tubular sodium reabsorption. These data support a significant role for elevated endogenous ANP in the maintenance of sodium excretion and regulation of the RAAS in experimental ELVD.

Aldosterone↗

PubMed1991

Experimental model of chronic global left ventricular dysfunction secondary to left coronary microembolization.

A model of chronic left ventricular dysfunction characterized by left ventricular dilation, elevated filling pressures and histologic changes has been lacking. In this study the use of coronary microsphere embolization-induced ischemia was explored as a method of producing chronic left ventricular dysfunction. Acute ischemic left ventricular dysfunction was induced in 13 mongrel dogs with 50 microns plastic microspheres until the peak positive first derivative of left ventricular pressure (dP/dt) decreased by 25% and the left ventricular end-diastolic pressure increased to greater than or equal to 12 mm Hg. After 8 weeks of observation, hemodynamic and echocardiographic variables were measured in each dog. Acute left ventricular dysfunction resulted in a dilated left ventricle with systolic dysfunction (area ejection fraction 24 +/- 6% vs. 57 +/- 9% initially, p less than 0.01) and elevated left ventricular filling pressures. Isovolumetric relaxation was prolonged and the peak rapid filling/atrial filling velocity and integral ratios were reduced. Eight weeks after embolization, there was an increased left ventricular size (end-diastolic area 15.1 +/- 2.1 cm2 at 8 weeks vs. 13.5 +/- 1.4 cm2 early after microsphere injection, p less than 0.05), unchanged end-systolic area, improved area ejection fraction and increased left ventricular mass. Left ventricular end-diastolic pressure increased and, despite continued abnormal relaxation, the peak rapid filling/atrial filling velocity and integral ratios increased to above baseline values, demonstrating a "restrictive" pattern. Gross and histologic examination revealed diffuse, patchy scarring associated with perivascular fibrosis. Thus, coronary microsphere embolization resulted in a model of chronic moderate left ventricular systolic dysfunction and abnormal diastolic function characterized by a "restrictive" filling pattern.

Animals↗

PubMed1997

Determinants of the pulmonary artery pressure rise in left ventricular dysfunction.

Pulmonary artery hypertension in patients with left ventricular dysfunction is related to poor outcome but the role of cardiac functional abnormalities in the genesis of pulmonary hypertension remains unknown. The aim of this prospective study was to identify the determinants of pulmonary hypertension in 102 consecutive patients with primary left ventricular dysfunction (ejection fraction < 50%). Systolic pulmonary artery pressure was measured by continuous wave Doppler. Left ventricular systolic and diastolic function, severity of functional mitral regurgitation, cardiac output, and left atrial volume were assessed using Doppler echocardiography. In patients with left ventricular dysfunction, systolic pulmonary artery pressure was increased (51 +/- 14 mmHg, range 23 to 87 mmHg). Mitral deceleration time (r = -0.61; p = 0.0001) and mitral effective regurgitant orifice (r = 0.50; p = 0.0001) were the strongest parameters related to systolic pulmonary artery pressure. Multivariate analysis identified these two variables as the strongest predictors of systolic pulmonary artery pressure in association with the mitral E/A ratio (p = 0.006) and age (p = 0.005). In conclusion, pulmonary hypertension is common and variable in patients with left ventricular dysfunction. It is closely related to diastolic dysfunction and severity of functional mitral regurgitation but not independently to the degree of left ventricular systolic dysfunction. These findings underline the importance of assessing diastolic function and quantifying mitral regurgitation in patients with left ventricular dysfunction.

Blood Pressure↗

PubMed2002

Aortic valve surgery in patients with left ventricular dysfunction.

Patient with advanced left ventricular dysfunction and heart failure symptoms, either secondary to severe aortic stenosis and a low transvalvular gradient, or chronic aortic insufficiency are sometimes referred for cardiac transplantation. Now, with improvements in both myocardial protection and better valve prostheses, aortic valve surgery for patients with even the most advanced ventricular dysfunction can be performed with low risk.

Adult↗

PubMed1997

Association of calcium channel blocker use with increased rate of acute myocardial infarction in patients with left ventricular dysfunction.

The Studies of Left Ventricular Dysfunction (SOLVD) assessed the effect of enalapril in patients with systolic left ventricular dysfunction (LVD). We performed retrospective analyses of the association between calcium channel blocker (CCB) use and fatal and nonfatal myocardial infarction (MI) in these patients. MI occurred in 11.5% of 845 patients receiving CCBs versus 7.5% of 2551 patients not receiving CCBs in the enalapril group and in 14.4% of 874 patients receiving CCBs versus 9.3% of 2527 patients not receiving CCBs in the placebo group. By multivariate Cox regression analysis, adjusting for comorbidity, cause and severity of LVD, heart failure, and concomitant drug use, CCB use was an independent predictor of MI (relative risk [RR] 1.37, confidence interval [CI] 1.14 to 1.63). The increase in MI risk was greater among patients with a higher heart rate (RR 1.46, CI 1.14 to 1.86) and lower blood pressure (RR 1.45, CI 1.14 to 1.86). The adjusted risk ratio for all-cause mortality associated with CCB use was 1.14 (CI 1.00 to 1.28; p = 0.0454). In this analysis of patients with LVD, CCB use was associated with significantly increased risk of fatal or nonfatal MI.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1991

Influence of acute right ventricular dysfunction on cardiac tamponade.

Echocardiographic and hemodynamic data were measured in nine closed chest dogs during graded cardiac tamponade (pericardial pressure 5, 10, 15 mm Hg) before and after production of diffuse acute ischemic right ventricular dysfunction. Right ventricular dysfunction was produced by intracoronary injection of nonradioactive microspheres (mean diameter +/- SD 54 +/- 4 microns) and caused a significant increase in right atrial pressure (7.6 +/- 1.4 vs. 1.6 +/- 1 mm Hg, p less than 0.001) and cross-sectional areas of both the right atrium (8.3 +/- 0.3 vs. 5.6 +/- 0.2 cm2, p less than 0.001) and right ventricle (8.8 +/- 0.4 vs. 5.7 +/- 0.4 cm2, p less than 0.001). Right atrial and ventricular collapse required a significantly larger pericardial effusion and pericardial pressure after right ventricular infarction than before. Mean aortic pressure had fallen 1.9 +/- 2% and 6.5 +/- 6.9% at the time of right atrial collapse (p = NS before vs. after right ventricular dysfunction) and 3 +/- 4.1% and 20.1 +/- 20.8% at the time of right ventricular collapse (p less than 0.03) before and after right ventricular dysfunction, respectively. In the presence of ischemic right ventricular dysfunction, echocardiographic signs of cardiac tamponade are less sensitive and occur later in the hemodynamic progression of cardiac tamponade. Pulsus paradoxus with cardiac tamponade was not prevented by coexisting ischemic right ventricular dysfunction.

Animals↗

PubMed1998

Relative efficacy of medical therapy and revascularization for improving exercise capacity in patients with chronic left ventricular dysfunction.

BACKGROUND: In patients with left ventricular dysfunction one of the aims of therapy may be to improve functional capacity. This study compared the improvement of functional capacity in response to medical therapy with that caused by revascularization. METHODS: Fifty-two patients with severe left ventricular dysfunction were divided into groups with ischemic cardiomyopathy undergoing revascularization (group A, n = 20) or incremental medical treatment (group B, n = 16) and a control group receiving maximal medical therapy at the start of the study (group C, n = 16). All patients underwent a baseline metabolic exercise test with evaluation of peak oxygen consumption and derived exercise capacity in metabolic equivalents (METS) with standard electrocardiographic and hemodynamic monitoring. Therapy was then optimized in the medical treatment group, whereas the revascularization group underwent coronary bypass grafting. All patients subsequently underwent follow-up metabolic exercise testing. RESULTS: In groups A, B, and C resting left ventricular ejection fractions were comparable (26%+/-5%, 25%+/-7%, and 23%+/-8%, respectively), as were results of initial metabolic exercise tests (4.7+/-0.9 METS, 4.7+/-1.4 METS, and 5.2+/-1.4 METS). At follow-up group A improved exercise capacity from 4.7 to 5.6 METS (p = 0.01). Groups B (4.7 to 5.0 METS) and C (5.2 to 5.6 METS) had no significant improvement. The mean respiratory exchange ratio improved significantly in group A (1.14 to 1.20, p = 0.02), as did left ventricular ejection fraction (26% to 31%, p = 0.02). However, neither parameter changed significantly in groups B or C. CONCLUSIONS: In patients with severe left ventricular dysfunction improvements of exercise capacity are more marked after coronary revascularization than may be obtained after maximization of medical therapy.

Adult↗

PubMed2002

Brain natriuretic peptide and left ventricular dysfunction in Chagas' disease.

Left ventricular dysfunction in Chagas' disease is common but can be difficult to detect. We investigated whether measurement of plasma brain natriuretic peptide (BNP) could identify patients with left ventricular dysfunction who need further investigation or treatment. Among patients with an abnormal electrocardiogram or chest radiograph, a BNP concentration of 60.7 pmol/L or higher has a sensitivity and positive predictive value of 80%, and specificity and negative predictive value of 97%. Measurement of plasma BNP concentration could be a useful method to screen patients with Chagas' disease.

Adult↗

PubMed1999

Relative effectiveness of the implantable cardioverter-defibrillator and antiarrhythmic drugs in patients with varying degrees of left ventricular dysfunction who have survived malignant ventricular arrhythmias. AVID Investigators. Antiarrhythmics Versus Implantable Defibrillators.

OBJECTIVES: We sought to assess the effect of baseline ejection fraction on survival difference between patients with life-threatening ventricular arrhythmias who were treated with an antiarrhythmic drug (AAD) or implantable cardioverter-defibrillator (ICD). BACKGROUND: The Antiarrhythmics Versus Implantable Defibrillators (AVID) study demonstrated improved survival in patients with ventricular fibrillation or ventricular tachycardia with a left ventricular ejection fraction (LVEF) < or =0.40 or hemodynamic compromise. METHODS: Survival differences between AAD-treated and ICD-treated patients entered into the AVID study (patients presenting with sustained ventricular arrhythmia associated with an LVEF < or =0.40 or hemodynamic compromise) were compared at different levels of ejection fraction. RESULTS: In patients with an LVEF > or =0.35, there was no difference in survival between AAD-treated and ICD-treated patients. A test for interaction was not significant, but had low power to detect an interaction. For patients with an LVEF 0.20 to 0.34, there was a significantly improved survival with ICD as compared with AAD therapy. In the smaller subgroup with an LVEF <0.20, the same magnitude of survival difference was seen as that in the 0.20 to 0.34 LVEF subgroup, but the difference did not reach statistical significance. CONCLUSIONS: These data suggest that patients with relatively well-preserved LVEF (> or =0.35) may not have better survival when treated with the ICD as compared with AADs. At a lower LVEF, the ICD appears to offer improved survival as compared with AADs. Prospective studies with larger patient numbers are needed to assess the effect of relatively well-preserved ejection fraction (> or =0.35) on the relative treatment effect of AADs and the ICDs.

Aged↗

PubMed1995

[Surgical results of aortic stenosis with or without left ventricular dysfunction--postoperative change of left ventricular function].

Between January 1980 and December 1992, 82 patients with aortic stenosis underwent isolated aortic valve replacement at our institution. Age of the patients ranged from 26 to 72 (58 +/- 6.4) years, and 58 were men and 24 were women. The patients were divided into two groups according to preoperative left ventricular ejection fraction (LVEF): 23 patients (LVEF < 50%, mean 39.7%; Group D) and 59 patients (LVEF > or = 50%, mean 62.6%; Group N). By means of echocardiography, LV function were evaluated before and at one month after operation in terms of left ventricular fractional shortening (LVFS), left ventricular systolic internal diameter (LVIDs), left ventricular mass index (LVMI), and left ventricular end systolic wall stress (ESWS). Postoperative early mortality including hospital death was 8.7% in group D (2 cases; myocardial infarction 1, cerebral complication 1) and 3.3% in group N (2 cases; myocardial infarction 1, low output syndrome 1), and this difference was not significant (NS) between two groups. The 5- and 12-year actuarial survival rate were 87.8% and 87.8% in group D, 91.5% and 87.6% in group N, respectively (NS). LVFS (pre/post) was 0.25 %/- 0/08/0.24 +/- 0.10 in group D, 0.38 +/- 0.10/0.32 +/- 0.10 in group N. The difference were significant before (p < 0.0005) and after (p < 0.005) operation between two groups. LVIDs (mm; pre/post) were 39.0 +/- 7.9/35.0 +/- 9.6 in group D, 28.7 +/- 7.3/229.3 +/- 7.6 in group N. The difference were significant before (p < 0.0005) and after (p < 0.01) operation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Valve replacement for regurgitant lesions of the aortic or mitral valve in advanced left ventricular dysfunction.

Patients with aortic regurgitation and severe left ventricular dysfunction remain candidates for aortic valve replacement, as long as the risks of late left ventricular dysfunction and congestive heart failure have been fully discussed with the patient, the patient's family, and the referring physician. In contrast, patients with mitral regurgitation and severe systolic dysfunction are at considerable risk of more severe left ventricular dysfunction after operation, especially if mitral valve repair or chordal-sparing procedure cannot be performed. In patients who are candidates for such procedures that preserve the integrity of the subvalvular mitral apparatus, operation may be successful in selected patients despite moderate-to-severe depression of systolic function. Prognosis is guarded to poor in patients with regurgitant valvular lesions and advanced left ventricular dysfunction, and the emerging alternative treatments discussed in other articles in this Cardiology Clinics deserve consideration in these patients.

Aortic Valve↗

PubMed1990

Preventive treatment of asymptomatic left ventricular dysfunction following myocardial infarction.

Progressive asymptomatic ventricular dilatation can occur following myocardial infarction and severe ventricular dysfunction is often present by the time clinical congestive heart failure occurs. In a randomized, double-blind trial, the effects of captopril 25 mg tid, frusemide 40 mg daily and placebo were studied in 90 patients with asymptomatic left ventricular dysfunction (ejection fraction less than 45%) 1 week following Q wave myocardial infarction. Left ventricular volumes and function were assessed at intervals during the subsequent year using two-dimensional echocardiography. The frusemide and placebo groups showed significant increases in ventricular volumes with stroke volume index unchanged and ejection fraction slightly reduced, whereas the captopril group showed a significant reduction in left ventricular end-systolic volume index with stroke volume index and ejection fraction increased. At 12 months the difference in the change in ejection fraction from baseline between the captopril and frusemide groups was 10.5% and captopril and placebo groups 9.6% (both P less than 0.0001). There was a significant difference in occurrence of clinical heart failure in the placebo group compared with the other groups (P less than 0.05). Blood pressure increased significantly within the normal range in the placebo and frusemide groups whereas there was essentially no change from baseline in the captopril group. There was no significant correlation between baseline left ventricular volumes and function and subsequent change, and anterior and inferior infarct subgroups showed similar responses within the treatment groups. In conclusion, captopril improves asymptomatic ventricular dysfunction and prevents clinical heart failure during the year following myocardial infarction. Frusemide may also prevent clinical heart failure but not progressive ventricular dilatation.

Adult↗

PubMed1992

Reversible left ventricular dysfunction induced by recurrent ventricular tachycardia.

Two cases of transient LV dysfunction associated with VT are described. Both patients had a history of palpitations of several years' duration without symptoms of congestive heart failure. The reason for presentation was an increase in frequency and duration of palpitation. Decreased LV wall motion, observed by 2DE, normalized shortly after treatment of the VT. Diffusely decreased LV wall motion is associated with frequent episodes of VT and may mimic DCM except that signs and symptoms of heart failure are absent.

Adult↗

PubMed1993

Changes in ventricular volume, wall thickness and wall stress during progression of left ventricular dysfunction. The SOLVD Investigators.

To assess the long-term changes in cardiac function in asymptomatic patients with severe left ventricular dysfunction, left ventricular (cineangiography) and right ventricular (radionuclide angiography) function were assessed at baseline in 49 patients enrolled in the prevention arm of the Studies of Left Ventricular Dysfunction. After an average follow-up period of 12.4 months, 30 patients (11 randomized to the placebo group and 19 to the enalapril group) could be restudied to assess the progression of ventricular dysfunction. After 1 year of follow-up, the changes in heart rate, left ventricular end-diastolic and systolic pressure and right ventricular volumes were comparable in both groups. However, there were modest but opposite changes in left ventricular end-diastolic volume (+9 ml/m2 with placebo vs. -10 ml/m2 with enalapril, p < 0.05) and end-systolic volume (+5 ml/m2 with placebo vs. -13 ml/m2 with enalapril, p < 0.05). Mean systolic wall stress increased insignificantly in both groups, whereas ejection fraction increased from 29% to 31% in the placebo group and from 28% to 32% with enalapril (p = NS, placebo vs. enalapril). Even in asymptomatic patients with severe left ventricular dysfunction, there was a slow progression of left ventricular dilation. Enalapril administration appeared to slow this progression, but wall stress was not normalized by the treatment at the doses used in the study, indicating that at least one of the stimuli for further remodeling remained present.

Adult↗