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PubMed1990

Comparison of neuroendocrine activation in patients with left ventricular dysfunction with and without congestive heart failure. A substudy of the Studies of Left Ventricular Dysfunction (SOLVD).

Neuroendocrine activation is known to occur in patients with congestive heart failure, but there is uncertainty as to whether this occurs before or after the presence of overt symptoms. In the Studies of Left Ventricular Dysfunction (SOLVD), a multicenter study of patients with ejection fractions of 35% or less, we compared baseline plasma norepinephrine, plasma renin activity, plasma atrial natriuretic factor, and plasma arginine vasopressin in 56 control subjects, 151 patients with left ventricular dysfunction (no overt heart failure), and 81 patients with overt heart failure before randomization. Median values for plasma norepinephrine (p = 0.0001), plasma atrial natriuretic factor (p less than 0.0001), plasma arginine vasopressin (p = 0.006), and plasma renin activity (p = 0.03) were significantly higher in patients with left ventricular dysfunction than in normal control subjects. Neuroendocrine values were highest in patients with overt heart failure. Plasma renin activity was normal in patients with left ventricular dysfunction without heart failure who were not receiving diuretics and was significantly increased (p less than 0.05) in patients on diuretic therapy. We conclude that neuroendocrine activation occurs in patients with left ventricular dysfunction and no heart failure. Neuroendocrine activation is further increased as overt heart failure ensues and diuretics are added to therapy.

Arginine Vasopressin↗
PubMed1994

Relation of neurohumoral activation to clinical variables and degree of ventricular dysfunction: a report from the Registry of Studies of Left Ventricular Dysfunction. SOLVD Investigators.

OBJECTIVES: This study examined the relation between neurohumoral activation and severity of left ventricular dysfunction and congestive heart failure in a broad group of patients with depressed left ventricular function who were not recruited on the basis of eligibility for a therapeutic trial. BACKGROUND: Previous studies have established the presence of neurohumoral activation in patients with severe congestive heart failure. It is not known whether the activation of these neurohumoral mechanisms is related to an impairment in left ventricular function. METHODS: From the 6,273 patients recruited into the Studies of Left Ventricular Dysfunction Registry (SOLVD), a subgroup of 859 patients were randomly selected, and their plasma norepinephrine, plasma renin activity, arginine vasopressin and atrial natriuretic peptide levels were correlated with clinical findings, New York Heart Association functional class, left ventricular ejection fraction and drug use. RESULTS: There was a weak but significant correlation between ejection fraction and an increase in plasma norepinephrine (rho = -0.18, p < 0.0001), plasma renin activity (rho = -0.24, p < 0.0001) and arginine vasopressin (rho = -0.12, p < 0.003). The only exception was atrial natriuretic peptide, which showed the best correlation to ejection fraction (rho = -0.37, p < 0.0001). Deterioration in functional class was associated more with increases in atrial natriuretic peptide (p = 0.0003) and plasma renin activity (p = 0.0003) and less with an increase in plasma norepinephrine. Of the clinical variables, elevated jugular venous pressure and third heart sound (S3) gallop were significantly associated with increased levels of plasma norepinephrine, plasma renin activity and atrial natriuretic peptide. We then compared the relation of neurohormones with clinical signs, functional status, ejection fraction and drug therapy and controlled for mutual interactive effects. After adjustment, a decrease in ejection fraction was still significantly related to an increase in plasma norepinephrine, plasma renin activity and atrial natriuretic peptide. In contrast, only a difference between functional classes I and III/IV was associated with an increase in plasma renin activity and atrial natriuretic peptide levels. CONCLUSIONS: Neurohumoral activation in patients with heart failure is related to severity of left ventricular functional depression, and this relation is independent of functional class or concomitant drug therapy.

Aged↗
PubMed1985

[Effect of aortocoronary bypass surgery on left ventricular function and coronary sinus blood flow in patients with severe left ventricular dysfunction].

Left ventricular function and coronary sinus blood flow were evaluated in 7 patients with severe left ventricular dysfunction at rest before and after aortocoronary bypass surgery, and during exercise after surgery. Same evaluations were performed in 8 normal subject (G-C). Cardiac index (CI) at rest (2.09 +/- 0.55 l/min/m2) significantly increased after operation (2.94 +/- 0.59 l/min/m2) (p less than 0.02). There was no difference between CI during exercise after operation (5.94 +/- 1.51 l/min/m2) and that in G-C. Left ventricular end-diastolic pressure (LVEDP) at rest before operation (16 +/- 8 mmHg) was significantly higher than that in G-C (p less than 0.05). This difference disappeared after operation. LVEDP during exercise after operation (25 +/- 10 mmHg) was significantly higher than that in G-C (p less than 0.01). Coronary sinus blood flow (CSF) at rest (73 +/- 15 ml/min) significantly increased after operation (123 +/- 44 ml/min) (p less than 0.02). There was no difference between CSF during exercise after operation (282 +/- 99 ml/min) and that in G-C. These data indicated that the aortocoronary bypass surgery was effective on left ventricular function and coronary sinus blood flow in patients with severe left ventricular dysfunction.

Adult↗
PubMed1994

Tolerability of enalapril initiation by patients with left ventricular dysfunction: results of the medication challenge phase of the Studies of Left Ventricular Dysfunction.

Although converting-enzyme inhibitors are useful for the treatment of congestive heart failure (CHF), there are concerns about adverse reactions especially on initiation of therapy. In the Studies of Left Ventricular Dysfunction, enalapril, 2.5 mg twice per day was given on an open-label outpatient basis for 7 days (mean 6.1, range 2 to 7, and median 7) as a prerandomization drug challenge to 7487 patients with left ventricular dysfunction (ejection fraction < or = 0.35). Four hundred forty-four (5.93%) patients reported side effects, including symptoms attributed to hypotension (in 166 patients [2.2%]). The majority (346 [77.9%] of 444 and 129 [77.7%] of 166 with symptoms attributed to hypotension) of patients who reported side effects were willing to participate in the study and to continue receiving enalapril. Thus only 98 (1.3%) of 7487 patients (0.5% because of symptoms attributed to hypotension) were not willing to continue because of side effects. Women and patients of CHF class III or IV were more likely to report side effects. In conclusion, enalapril is well tolerated by patients with left ventricular dysfunction; treatment can be initiated on an outpatient basis in the majority of patients.

Enalapril↗
PubMed1997

Attenuation of unfavorable remodeling by exercise training in postinfarction patients with left ventricular dysfunction: results of the Exercise in Left Ventricular Dysfunction (ELVD) trial.

BACKGROUND: Exercise is currently recommended for patients after myocardial infarction; however, the effects of regular exercise on the remodeling process remain to be defined. The aim of this multicenter, randomized study was to investigate whether a long-term physical training program influences left ventricular size and function in postinfarction patients with systolic dysfunction. METHODS AND RESULTS: Consecutive patients with <40% ejection fraction after a first Q-wave myocardial infarction were randomly assigned to a 6-month exercise training program (n=39) or control group (n=38). After 6 months, a significant increase in work capacity was observed only in the training group (from 4.462+/-1.095 to 5.752+/-1.749 kilopond-meters [Kp-m], P<.01), not in the control group (from 4.375+/-1.143 to 4.388+/-1.199 Kp-m), whereas left ventricular volumes had increased in the control group (end-diastolic volume, from 94+/-26 to 99+/-27 mL/m2, P<.01; end-systolic volume, from 62+/-20 to 67+/-23 mL/m2, P<.01) but not in the training group (end-diastolic volume, from 93+/-28 to 92+/-28 mL/m2, P=NS; end-systolic volume, from 61+/-22 to 57+/-23 mL/m2, P=NS). Conversely, ejection fraction had improved in the training group (from 34+/-5% to 38+/-8%, P<.01) but not in the control group (from 34+/-5% to 33+/-7%, P=NS). CONCLUSIONS: In postinfarction patients with systolic dysfunction, long-term exercise training may attenuate the unfavorable remodeling response and even improve ventricular function over time.

Adult↗
PubMed2000

Echocardiographic predictors of clinical outcome in patients with left ventricular dysfunction enrolled in the SOLVD registry and trials: significance of left ventricular hypertrophy. Studies of Left Ventricular Dysfunction.

OBJECTIVES: To assess the relation of left ventricular (LV) and left atrial (LA) dimensions, ejection fraction (EF) and LV mass to subsequent clinical outcome of patients with LV dysfunction enrolled in the Studies of Left Ventricular Dysfunction (SOLVD) Registry and Trials. BACKGROUND: Data are lacking on the relation of LV mass to prognosis in patients with LV dysfunction and on the interaction of LV mass with other measurements of LV size and function as they relate to clinical outcome. METHODS: A cohort of 1,172 patients enrolled in the SOLVD Trials (n = 577) and Registry (n = 595) had baseline echocardiographic measurements and follow-up for 1 year. RESULTS: After adjusting for age, New York Heart Association (NYHA) functional class, Trial vs. Registry and ischemic etiology, a 1-SD difference in EF was inversely associated with an increased risk of death (risk ratio, 1.62; p = 0.0008) and cardiovascular (CV) hospitalization (risk ratio, 1.59; p = 0.0001). Consequently, the other echo parameters were adjusted for EF in addition to age, NYHA functional class, Trial vs. Registry and ischemic etiology. A 1-SD difference in LV mass was associated with increased risk of death (risk ratio of 1.3, p = 0.012) and CV hospitalization (risk ratio of 1.17, p = 0.018). Similar results were observed with the LA dimension (mortality risk ratio, 1.32; p < 0.02; CV hospitalizations risk ratio, 1.18; p < 0.04). Likewise, LV mass > or =298 g and LA dimension > or =4.17 cm were associated with increased risk of death and CV hospitalization. An end-systolic dimension >5.0 cm was associated with increased mortality only. A protective effect of EF was noted in patients with LV mass > or =298 g (those in the group with EF >35% had lower mortality) but not in the group with LV mass <298 g. CONCLUSIONS: In patients with LV dysfunction enrolled in the SOLVD Registry and Trials, increasing levels of hypertrophy are associated with adverse events. A protective effect of EF was noted in patients with LV mass > or =298 g (those in the group with EF >35% fared better) but not in the group with LV mass <298 g. These data support the development and use of drugs that can inhibit hypertrophy or alter its characteristics.

Aged↗
PubMed1995

Use of electrophysiological studies in the diagnosis and treatment of cardiac patients with left ventricular dysfunction and high grade ventricular ectopy.

We studied the sudden death occurrence in 28 patients (23 males, age 59.2 +/- 15.6 years) who had a documented cardiac disease with left ventricular dysfunction (ejection fraction < or = 0.4) and high grade ventricular ectopy. None had suffered from spontaneous sustained ventricular arrhythmia and/or syncope. Their diagnosis and treatment were guided by electrophysiological studies. Electrophysiological studies were performed in the antiarrhythmic drug-free state. In cases when sustained ventricular arrhythmias could be induced, antiarrhythmic treatment was prescribed according to the results of the electrophysiological studies. In cases of non-inducibility, no antiarrhythmic treatment was prescribed. The patients were followed up for a period of 20.6 +/- 11.2 months. The end points were occurrence of documented spontaneous sustained ventricular arrhythmia and sudden death. None of the 19 non-inducible patients experienced sudden death or spontaneous sustained ventricular arrhythmia. Two of the nine inducible patients died suddenly (P = 0.1). The 3-year sudden death mortality rate of the whole group was 7.5%. We conclude that when cardiac patients with high grade ventricular ectopy and left ventricular systolic dysfunction are treated according to the results of electrophysiological studies, it can be expected that their 3-year mortality rate will be low and significantly inferior to that reported for conventionally treated patients.

Adult↗
PubMed1988

Left ventricular dysfunction due to chronic right ventricular pressure overload. Resolution following percutaneous balloon valvuloplasty for pulmonic stenosis.

Left ventricular dysfunction due to chronic right ventricular pressure overload is well documented in experimental animals, but is controversial in humans. Whether left ventricular dysfunction resolves following the relief of chronic right ventricular pressure overload has not been studied. In this report, rapid improvement in both right and left ventricular function following successful percutaneous balloon valvuloplasty is described in a patient with severe isolated valvular pulmonic stenosis and biventricular dysfunction. It appears that: (1) geometric distortion played a major role in his reversible left ventricular dysfunction, and (2) severe biventricular dysfunction should not be a contraindication to valvuloplasty for valvular pulmonic stenosis.

Adult↗
PubMed1981

Right ventricular dysfunction in acute ventricular septal defect.

Eight patients with acute ventricular septal defect (VSD) receiving early intra-aortic balloon augmentation, cardiac catheterization, and open-heart surgery are described. Because of the large shunts in this group of patients, there was visualization of the right ventricle during left ventriculography which was adequate for qualitative analysis. The following were noted: (1) All patients had severe right ventricular (RV) dysfunction angiographically. (2) RV akinesis noted on angiography was more extensive than the surgical description of RV infarction, although all patients had biventricular infarction at surgery. (3) The RV dysfunction was the major cause of death (two cases) or a contributing factor (three cases). (4) RV papillary muscle rupture was identified in one case.

Acute Disease↗
PubMed1988

Conventional and right precordial ECGs, creatine kinase, and radionuclide angiography in post-traumatic ventricular dysfunction.

Right ventricular infarction due to ischemic heart disease can be diagnosed by a right precordial electrogram or by first-pass radionuclide angiography (FPRNA). Prior FPRNA studies have shown that cardiac dysfunction after blunt chest trauma (myocardial contusion) is most often due to right ventricular dysfunction. We hypothesized that right ventricular dysfunction due to ischemic heart disease and myocardial contusion should produce similar ECG changes due to myocyte disruption. The purpose of our study was to evaluate the diagnostic value of the right precordial electrogram in suspected cardiac contusion. Thirty-five patients with suspected myocardial contusion based on mechanism of injury/clinical findings and no history of clinical heart disease were enrolled prospectively. All patients had conventional ECG, right precordial electrogram, and FPRNA studies. Twenty patients had normal cardiac scans (group 1); percentage of myocardial creatine kinase (CK-MB) was measured in 12 of these patients and was less than 5% in 11. Fifteen patients had abnormal cardiac scans (wall motion abnormality and/or decreased right ventricular ejection fraction) (mean, 34% +/- 7% [SD]; normal, greater than 40%) (group 2); percentage of CK-MB was measured in 13 of 15 patients and was less than 5% in all 13. Conventional ECGs and right precordial electrograms in all patients were analyzed for differences in heart rate, PR interval, QRS duration, corrected QT interval, and the axis of the frontal and horizontal plane QRS complex and ST segment. There were no significant differences between group 1 and group 2 patients. No patient with myocardial contusion diagnosed by FPRNA had elevated ST segments in V4R through V6R or a percentage CK-MB of more than 5%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

Late survival after valve operation in patients with left ventricular dysfunction.

BACKGROUND: Left ventricular dysfunction is a predictor of hospital mortality after cardiac valve operation. We evaluated late survival in a large cohort of these patients. METHODS: From 1980 to 1993, 257 patients with a preoperative ejection fraction of 0.40 or less underwent aortic (n = 177), mitral (n = 72), or combined (n = 8) valve operation, with or without concomitant coronary artery bypass grafting. RESULTS: Hospital mortality was 12.5%. Follow-up was 98% complete. Logistic regression analysis showed that an ejection fraction of less than 0.30, mitral regurgitation, concomitant coronary artery bypass grafting, emergency operation, and reoperation were independent correlates of hospital mortality (all at p < 0.05). Kaplan-Meier survival curves of the 220 hospital survivors showed a 65% 5-year survival. Multivariate analysis revealed preoperative use of diuretics, male sex, reoperation, age exceeding 60 years, and aortic regurgitation to be independent predictors of poor late outcome (all at p < 0.05). CONCLUSIONS: The liability of left ventricular dysfunction with regard to diminished long-term survival is not completely reversed by valve operation. If operation is not performed before left ventricular dysfunction develops, postoperative medical treatment of these dilated, remodeled ventricles should be considered.

Adolescent↗
PubMed1996

Angina and left ventricular dysfunction.

Angina with left ventricular dysfunction exhibits a wide range of different presentations. Approximately 45% of patients referred for coronary artery bypass surgery have some degree of left ventricular dysfunction and, given that at least a third of those suffering from angina have a history of myocardial infarction, the prevalence of left ventricular dysfunction in such patients is likely to be substantial. The major prognostic factor in patients with coronary artery disease is the degree of left ventricular function and it is important to identify those with poor or reduced left ventricular function. High-risk patients, defined by exercise testing and echocardiography, should be considered for revascularization. For the majority of patients management should be medical, consisting of nitrates plus a beta-blocker or calcium antagonist. In severe ischaemia, the combination of these agents has been shown to provide additional efficacy. In patients with heart failure the newer calcium antagonist amlodipine has been shown to have a neutral effect upon survival, indicating that it may be used safely in patients with angina and left ventricular dysfunction. Progression of left ventricular dysfunction may be slowed through the use of angiotensin converting enzyme (ACE) inhibitors, which have also been shown to improve survival, although they should be used with caution, since there is evidence that ACE inhibitors may worsen angina in some patients.

Angina Pectoris↗
PubMed1987

Stress induced right ventricular dysfunction: an indication of reversible right ventricular ischaemia.

Stress induced changes in left ventricular ejection fraction are widely used in the detection and assessment of coronary artery disease. This study demonstrates that right ventricular dysfunction may also occur, and assesses its significance in terms of coronary artery anatomy. This study involved 14 normal subjects and 26 with coronary artery disease investigated by equilibrium radionuclide ventriculography, at rest and during maximal dynamic exercise. Mean normal resting right ventricular ejection fraction (RVEF) was 0.40 (SD 0.118), and all normal subjects increased RVEF with stress (mean delta RVEF + 0.13 SD 0.099). Mean delta RVEF in the subjects with coronary artery disease was significantly lower at 0.00 (SD 0.080), but there was overlap between the two groups. The largest falls in RVEF were seen if the right coronary artery was occluded without retrograde filling. In this subgroup with the most severely compromised right ventricular perfusion (nine subjects), RVEF always fell with stress, and mean delta RVEF was -0.08 (SD 0.050). There was no significant correlation between delta LVEF and delta RVEF, implying that the right ventricular dysfunction was due to right ventricular ischaemia, rather than secondary to left ventricular dysfunction. Stress induced right ventricular ischaemia can therefore be detected readily by radionuclide ventriculography.

Adult↗
PubMedDate not supplied

Spontaneous resolution of severe right ventricular dysfunction in right ventricular infarction: documentation by radionuclide studies.

A case of inferior myocardial infarction complicated by severe arrhythmias and right heart failure is presented. Radionuclide studies performed near the acute phase and one month later illustrate the reversibility of right heart dysfunction caused by infarction. Signs of right ventricular involvement in acute inferior myocardial infarction are noted in about 40% of cardiac blood-pool studies: right ventricular dilatation with a significantly decreased ejection fraction, and ventricular wall motion abnormalities. Follow-up studies in the recovery period show good recovery of right ventricular function.

Aged↗
PubMed1992

Comparison of painful and painless left ventricular dysfunction recorded during ambulatory ventricular function monitoring in angina pectoris secondary to coronary artery disease.

Left ventricular (LV) function and the electrocardiogram of 55 patients with coronary artery disease and angina were monitored for a mean of 3.2 +/- 1.9 hours with an ambulatory LV function monitor. During the monitoring interval, patients performed daily activities such as sitting, walking, climbing stairs, and eating. Sixty episodes of transient reduction in ejection fraction of > 5% lasting > 60 seconds were observed in 24 patients; 13 episodes were associated with typical angina, but 47 were asymptomatic. Asymptomatic episodes had a shorter duration of ventricular dysfunction (116 +/- 49 vs 189 +/- 113 seconds; p < 0.05), and smaller increases in relative end-diastolic and end-systolic volumes (end-diastolic 0.9 +/- 5.4% vs 4.6 +/- 4.9% [p < 0.05], and end-systolic 21 +/- 11% vs 35 +/- 20% [p < 0.05]) than did symptomatic ones. When a subset of patients with both symptomatic and asymptomatic episodes were analyzed, similar results were observed: in asymptomatic episodes, duration was shorter (82 +/- 31 vs 200 +/- 110 seconds; p < 0.005), ejection fraction decrease was smaller (-7.3 +/- 2.6% vs -11.0 +/- 4.7%; p < 0.05), and end-systolic volume increase was smaller (23 +/- 12% vs 37 +/- 19%; p < 0.05). The data suggest that asymptomatic transient LV dysfunction is less severe and of shorter duration in patients with angina pectoris.

Angina Pectoris↗
PubMed2000

Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction.

OBJECTIVE: Rapid ventricular pacing produces a reliable model of heart failure. Cessation after 4 weeks of rapid ventricular pacing results in rapid normalization of left ventricular function, but the left ventricle remains persistently dilated. We present novel data that show that prolonged rapid ventricular pacing (10 weeks) creates a model of chronic left ventricular dysfunction. METHODS: In 9 dogs undergoing 10 weeks of rapid ventricular pacing, left ventricular function and volumes were serially assessed by using 2-dimensional echocardiography and pressure-volume analysis for 12 weeks after cessation of pacing. RESULTS: Increased end-diastolic volume and decreased systolic and diastolic function were seen at the end of pacing. By 2 weeks of recovery from rapid ventricular pacing, end-diastolic volume and ejection fraction were partially recovered but did not improve further thereafter. Load-independent and load-sensitive indices of function obtained by pressure-volume analysis at 8 and 12 weeks of recovery confirmed a persistence of both systolic and diastolic dysfunction. In addition, left ventricular mass increased with pacing and remained elevated at 8 and 12 weeks of recovery. Four of these dogs studied at 6 months of recovery showed similar left ventricular abnormalities. CONCLUSION: Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction.

Animals↗
PubMed1980

Ventricular compliance in ischemic right ventricular dysfunction.

Ischemic right ventricular dysfunction was diagnosed in 54 patients with acute myocardial infarction who had a right atrial pressure disproportionately increased in relation to the pulmonary capillary pressure. The right atrial pressure curve in 40 patients (74 percent) was M- or W-shaped, termed a noncompliant pattern, and was similar to the pattern found in constrictive pericarditis. Kussmaul's sign was found in the patients whose respiration was recorded. This pattern, which represents poor right ventricular compliance, was severe in 30 cases (y descent greater than x descent) and slight in 10 cases (y descent = x descent). Its duration was variable, ranging from days to years. Of the 54 patients, 32 (59 percent) had a low output syndrome, diagnosed in the presence of a cardiac index of less than 2.2 liters/min per m2, with signs of poor tissue perfusion. The severe noncompliant pattern was significantly related to the presence of a low output syndrome (p less than 0.01) and mortality from this cause (p less than 0.05). The jugular venous tracing pulse had a pattern similar to that of the right atrial pressure recording and therefore may be valuable in the noninvasive diagnosis of right ventricular dysfunction and in the study of the evolution of the noncompliant pattern and, hence, of ventricular compliance.

Acute Disease↗