Serial observations on left ventricular dysfunction in acute myocardial infarction. I. Gallop sounds, ventricular asynergy and radiological signs.
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Acute Disease↗
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Prevalence and prognostic value of left ventricular dysfunction in non-Q-wave myocardial infarction.
Forty-two consecutive patients with non-Q-wave acute myocardial infarction (AMI) and 40 consecutive patients with transmural AMI were comparatively examined by equilibrium gated radionuclide angiography (ERNA) to assess prevalence and prognostic value of left ventricular dysfunction in non-Q-wave AMI. Left ventricular ejection (LVEF) was generally preserved both in anterior and inferior non-Q-wave infarctions and sharply reduced only in anterior transmural infarctions. ERNA cannot assist in identifying any subgroup of patients with non-Q-wave AMI at risk of major complications other than left ventricular failure because they may develop such complications in spite of a normal LVEF.
Adult↗
Differences in mechanisms and outcomes of syncope in patients with coronary disease or idiopathic left ventricular dysfunction as assessed by electrophysiologic testing.
OBJECTIVES: This study evaluated the causes of syncope and the significance and differences in left ventricular (LV) dysfunction, coronary disease, and idiopathic dilated cardiomyopathy (DCM). BACKGROUND: Risk stratification of and indications for an automated defibrillator could differ according to the cause of LV dysfunction. METHODS: Electrophysiologic study, including atrial and ventricular programmed stimulation, was performed in 119 patients with coronary disease (group I) and 61 patients with DCM (group II) with an left ventricular ejection fraction (LVEF) <40% and syncope. Patients were followed from one to six years (mean 4 +/- 2 years). RESULTS: Sustained monomorphic ventricular tachycardia (VT) was induced in 44 group I patients (37%) and 13 group II patients (21%); ventricular flutter (>270 beats/min) or ventricular fibrillation (VF) was induced in 24 group I patients (19%) and 9 group II patients (15%); and various other arrhythmias were identified. Syncope remained unexplained in 34 group I patients (30%) and 16 group II patients (27%). Prognosis depended on the heart disease: VT or VF induction was a predictive factor of mortality in coronary disease and identified a group with high cardiac mortality (46%), compared with patients with a negative study, who had a lower mortality (6%; p < 0.001) than in other studies. Cardiac mortality was only correlated with LVEF in DCM. CONCLUSIONS: Various causes could explain syncope in 70% of patients with coronary disease and DCM, but differences were noted: VT was frequent in coronary disease with a bad prognosis, and ischemia could explain syncope; in DCM, different causes such as atrial tachycardia could be responsible for syncope, but the prognosis only depended on LVEF.
Aged↗
Current and ongoing randomized trials in heart failure and left ventricular dysfunction.
Several large randomized trials have been completed recently and provided valuable information on the effects of various interventions in heart failure and left ventricular dysfunction. A review of ongoing randomized trials showed that there were 19 major trials addressing the effect of treatments on exercise tolerance, morbidity or mortality. Although it is hoped that these trials will answer many questions, they will also raise additional questions. Therefore, these remaining questions will need to be answered by future clinical trials.
Adrenergic beta-Antagonists↗
Serial evaluation of right ventricular dysfunction associated with acute inferior myocardial infarction.
Right ventricular (RV) function was evaluated serially by multigated blood pool imaging in 18 patients with RV dysfunction associated with acute inferior myocardial infarction. Radionuclide ventriculograms were performed on all patients within 18 hours of chest pain and again at 10 days. In addition, 15 of 18 patients had rest and exercise radionuclide ventriculograms at 3 months. The mean resting right ventricular ejection fractions (RVEF) at admission, 10 days, and 3 months in these patients was 31.8 +/- 12.6% (SD), 46.9 +/- 11.2% (p less than 0.05), and 44.5 +/- 10.2% (p less than 0.05), while the left ventricular ejection fractions were 55.9 +/- 10.6%, 57.9 +/- 13.3%, and 53.1 +/- 11.2% (p = ns). The 3-month exercise radionuclide ventriculogram demonstrated an increase in RVEF greater than 5% in 6 of 15 patients. In eight catheterized patients, neither the location nor the severity of coronary artery narrowing nor the presence of collaterals correlated with the RV exercise response. Improvement in RV function over a 10-day interval following acute inferior myocardial infarction suggests the presence of significant reversible right ventricular dysfunction during the acute phase.
Cardiac Catheterization↗
Treatment with enalapril fails to prevent impaired cardiopulmonary baroreflex control in dogs with left ventricular dysfunction.
That the cardiopulmonary baroreflex control of sympathetic nerve activity is impaired in dogs with left ventricular (LV) dysfunction has been shown previously. This study tested the hypothesis that treatment with the angiotensin-converting enzyme inhibitor enalapril prevents or delays the development of abnormalities of cardiopulmonary baroreflexes in dogs with LV dysfunction. Serial changes in LV volumes and neurohumoral profiles (plasma norepinephrine and renin activity) were assessed in conscious dogs with progressive LV dysfunction due to rapid ventricular pacing. Enalapril 5 mg orally twice daily was administered from days 4 to 12 of pacing. Cardiopulmonary baroreflexes were assessed in enalapril-treated paced dogs (n = 8) and untreated paced dogs (n = 8) by recording changes in renal nerve activity and pulmonary capillary wedge pressure during volume infusion in anesthetized sinoaortic denervated dogs on day 12 of rapid pacing. There was no difference in LV volume in the two groups. Neurohumoral factors were similar in both groups except for the expected high plasma renin activity in enalapril-treated dogs. Hemodynamic parameters also were comparable in the two groups. Cardiopulmonary baroreflex sensitivity for enalapril-treated dogs was not different from that of untreated paced dogs, and baroreflex gain in both groups was significantly lower than for the nonpaced control dogs (P < .05). Despite adequate converting enzyme blockade, treatment with enalapril failed to prevent the development of attenuated cardiopulmonary baroreflex control of sympathetic nerve activity in dogs with developing LV dysfunction.
Angiotensin-Converting Enzyme Inhibitors↗
Cardiovascular and neurohormonal effects of atrial natriuretic peptide in conscious dogs with and without chronic left ventricular dysfunction.
Atrial natriuretic peptide (hANP 4-28) was infused for 1 h (0.3 microgram/kg/min) in 11 normal awake dogs and seven awake dogs with chronic left ventricular dysfunction, induced 16 weeks earlier by repetitive DC shock. The responses were similar in the two groups and included decreases in arterial pressure (107-99 mm Hg), heart rate (83-72 beats/min), and cardiac output (3.6-2.8 L/min), without changes in right or left ventricular filling pressures. Systemic vascular resistance (SVR) tended to rise during the infusion and was significantly increased (2,847-3,442 dyn s cm-5, p less than .05) during the postinfusion recovery period. Regional blood flows (microspheres) during infusion revealed a decrease in skin and splanchnic flow. Despite the apparent vasoconstrictor effect, plasma norepinephrine (PNE), renin activity (PRA), and arginine vasopressin (AVP) levels all fell during ANP infusion. These data suggest that ANP exerts a cardioinhibitory effect, possibly similar to that of arginine vasopressin (AVP), and that the net systemic vasoconstrictor effect of ANP in these dogs is mediated by a complex interrelationship between direct vascular effects, neurohormonal inhibition, and central reflex activation.
Animals↗
Effect of indecainide in patients with left ventricular dysfunction.
Indecainide, a new antiarrhythmic agent classified as type Ic was evaluated in 11 patients with heart disease who had greater than or equal to 30 ventricular premature complexes/hour, moderate-to-marked left ventricular dysfunction, and mean ejection fraction 34% +/- 8%. Patients received indecainide, 50 mg by mouth, every 6 hours and the dose was increased until greater than or equal to 80% suppression was noted, adverse effects occurred, or a maximum dose of 100 mg indecainide was given every 6 hours. Ventricular premature complexes were suppressed greater than or equal to 80% in nine patients (p less than 0.05) and ventricular tachycardia episodes were completely suppressed in five of eight patients. The effective or maximal mean daily indecainide dose was 191 +/- 32 mg; half of the responders achieved achieved efficacy at serum drug concentration greater than or equal to 600 ng/ml. Serum drug concentration was directly related to gender (r = 0.78, p less than 0.04) and inversely related to creatinine clearance (r = 0.74, p less than 0.05) and ejection fraction (r = 0.71, p less than 0.02). Indecainide prolonged mean PR and QRS intervals (p less than 0.05) but not QT or QTc. There was a linear relation between percent change in PR (r = 0.80, p less than 0.001) and QRS (r = 0.66, p less than 0.001) intervals and serum drug concentration. After starting or increasing the dose, careful observation of patients with decreased renal function or reduced ejection fraction should be exercised because they attain higher drug concentration than normal subjects.
Adult↗
"Escape" of aldosterone production in patients with left ventricular dysfunction treated with an angiotensin converting enzyme inhibitor: implications for therapy.
Despite the findings in randomized trials of a significant effect of angiotensin-converting enzyme (ACE) inhibitors in reducing morbidity and mortality of patients with symptomatic left ventricular dysfunction, the morbidity and mortality of these patients remains relatively high. One potential strategy to further improve morbidity and mortality in these patients is blockade of a aldosterone. Many clinicians have assumed that ACE inhibitors would block both angiotensin II and aldosterone. However, there are data to suggest that aldosterone production may "escape" despite the use of an ACE inhibitor. An escape of aldosterone production has several important consequences, including: sodium retention, potassium and magnesium loss, myocardial collagen production, ventricular hypertrophy, myocardial norepinephrine release, endothelial dysfunction, and a decrease in serum high density lipoprotein cholesterol. Due to the potential importance of these mechanisms, the finding that there is a significant correlation between aldosterone production and mortality in patients with heart failure, as well as evidence that an aldosterone antagonist, spironolactone, when administered to patients with heart failure treated with conventional therapy including an ACE inhibitor results in increased diuresis and symptomatic improvement, an international prospective multicenter study has been organized, the Randomized Aldactone Evaluation Study (RALES Pilot Study), to evaluate the safety of blocking the effects of aldosterone in patients with heart failure treated with an ACE inhibitor.
Aldosterone↗
Biochemical diagnosis of ventricular dysfunction in elderly patients in general practice: observational study.
OBJECTIVE: To investigate the usefulness of measuring plasma concentrations of B type natriuretic peptide in the diagnosis of left ventricular systolic dysfunction in an unselected group of elderly people. DESIGN: Observational study. SETTING: General practice with four centres in Poole, Dorset. PARTICIPANTS: 155 elderly patients aged 70 to 84 years. MAIN OUTCOME MEASURES: Diagnostic characteristics of plasma B type natriuretic peptide measured by radioimmunoassay as a test for left ventricular systolic dysfunction assessed by echocardiography. RESULTS: The median plasma concentration of B type natriuretic peptide was 39.3 pmol/l in patients with left ventricular systolic dysfunction and 15.8 pmol/l in those with normal function. The proportional area under the receiver operator curve was 0.85. At a cut-off point of 18.7 pmol/l the test sensitivity was 92% and the predictive value 18%. CONCLUSIONS: Plasma concentration of B type natriuretic peptide could be used effectively as an initial test in a community screening programme and, possibly, using a low cut-off point, as a means of ruling out left ventricular systolic dysfunction. It is, however, not a good test to "rule in" the diagnosis, and access to echocardiography remains essential for general practitioners to diagnose heart failure early.
Aged↗
Right ventricular dysfunction in chronic heart failure patients.
AIM: To evaluate any differences in haemodynamic and echocardiographic parameters in patients with both left (LV) and right ventricular (RV) systolic dysfunction and in patients with isolated LV systolic dysfunction. STUDY GROUP: One hundred patients with RV systolic dysfunction defined as peak velocity of tricuspid annular motion in systole (Sa)<11.5 cm/s, and 55 patients without RV systolic dysfunction Sa>11.5 cm/s. All patients had LV systolic dysfunction, LV ejection fraction (EF) below 40%, NYHA II-IV. METHODS: LV diameters, volumes and EF were measured by echocardiography. Patients underwent tissue Doppler imaging (TDI) of tricuspid annular motion with measurement of peak systolic velocity (Sa), peak early (Ea) and peak late (Aa) diastolic velocities. Right heart catheterization was also performed. RESULTS: Patients with RV systolic dysfunction did not differ from those without RV systolic dysfunction in terms of LV function. Patients with RV systolic dysfunction had larger RV dimension 30.6+/-5.8 vs. 33.9+/-6.7 mm, p<0.002. The patients with RV systolic dysfunction had higher values on right heart catheterization: MPAP 29.6+/-12.1 vs. 24.9+/-11.4 mm Hg, p<0.02, PCWP 20.8+/-10.0 vs. 17.3+/-9.3 mm Hg, p<0.03, PVR 189.9+/-123.3 vs. 137.7+/-94.9 dyn s cm(-5), p<0.008, CVP 7.7+/-5.6 vs. 5.1+/-3.9 mm Hg, p<0.002. The patients with RV systolic dysfunction had more pronounced diastolic dysfunction measured by TDI: Ea 9.9+/-2.3 vs. 11.4+/-2.5 cm/s, p<0.0001 and Aa 13.1+/-4.0 vs. 16.5+/-4.7 cm/s, p<0.000007. CONCLUSION: Patients with heart failure and both left and right ventricular systolic dysfunction showed more serious findings on central haemodynamics as well as more pronounced right ventricular diastolic dysfunction than those with isolated left ventricular systolic dysfunction.
Female↗
Myocardial injury and ventricular dysfunction related to training levels among nonelite participants in the Boston marathon.
BACKGROUND: Multiple studies have individually documented cardiac dysfunction and biochemical evidence of cardiac injury after endurance sports; however, convincing associations between the two are lacking. We aimed to determine the associations between the observed transient cardiac dysfunction and biochemical evidence of cardiac injury in amateur participants in endurance sports and to elicit the risk factors for the observed injury and dysfunction. METHODS AND RESULTS: We screened 60 nonelite participants, before and after the 2004 and 2005 Boston Marathons, with echocardiography and serum biomarkers. Echocardiography included conventional measures as well as tissue Doppler-derived strain and strain rate imaging. Biomarkers included cardiac troponin T (cTnT) and N-terminal pro-brain natriuretic peptide (NT-proBNP). All subjects completed the race. Echocardiographic abnormalities after the race included altered diastolic filling, increased pulmonary pressures and right ventricular dimensions, and decreased right ventricular systolic function. At baseline, all had unmeasurable troponin. After the race, > 60% of participants had increased cTnT > 99th percentile of normal (> 0.01 ng/mL), whereas 40% had a cTnT level at or above the decision limit for acute myocardial necrosis (> or = 0.03 ng/mL). After the race, NT-proBNP concentrations increased from 63 (interquartile range [IQR] 21 to 81) pg/mL to 131 (IQR 82 to 193) pg/mL (P<0.001). The increase in biomarkers correlated with post-race diastolic dysfunction, increased pulmonary pressures, and right ventricular dysfunction (right ventricular mid strain, r=-0.70, P<0.001) and inversely with training mileage (r=-0.71, P<0.001). Compared with athletes training > 45 miles/wk, athletes who trained < or = 35 miles/wk demonstrated increased pulmonary pressures, right ventricular dysfunction (mid strain 16+/-5% versus 25+/-4%, P<0.001), myocyte injury (cTnT 0.09 versus < 0.01 ng/mL, P<0.001), and stress (NT-proBNP 182 versus 106 pg/mL, P<0.001). CONCLUSIONS: Completion of a marathon is associated with correlative biochemical and echocardiographic evidence of cardiac dysfunction and injury, and this risk is increased in those participants with less training.
Athletic Injuries↗
Antiplatelet agents and survival: a cohort analysis from the Studies of Left Ventricular Dysfunction (SOLVD) trial.
OBJECTIVES: This study sought to evaluate the relation between antiplatelet agent (APA) use and survival and morbidity from cardiac disease in patients with left ventricular (LV) systolic dysfunction. BACKGROUND: APAs play an important role in the prevention and treatment of coronary disease. Their effects in patients with LV systolic dysfunction are unknown. METHODS: We reviewed data on APA use in 6,797 patients enrolled in the Studies of Left Ventricular Dysfunction (SOLVD) trial and analyzed the relation between their use and all-cause mortality as well as the combined end point of death or hospital admission for heart failure (HF). We used Cox regression to adjust for differences in baseline characteristics and to test for the interaction between APA use and selected patient variables in relation to outcome. RESULTS: APA use (46.3% of patients) was associated with significantly reduced mortality from all causes (adjusted hazard ratio [HR] 0.82, 95% confidence interval [CI] 0.73 to 0.92, p = 0.0005) and reduced risk of death or hospital admission for HF (adjusted HR 0.81, 95% CI 0.74 to 0.89, p < 0.0001) but was not influenced by trial assignment, gender, LV ejection fraction, New York Heart Association class or etiology. A strong interaction was observed among APA use, randomization group and all-cause mortality. The association between APA use and survival was not observed in the enalapril group, nor was an enalapril benefit on survival detectable in patients receiving APAs at baseline. However, randomization to enalapril therapy significantly reduced the combined end point of death or hospital admission for HF in APA users. CONCLUSIONS: In patients with LV systolic dysfunction, use of APAs is associated with improved survival and reduced morbidity. This association is retained after adjustment for baseline characteristics. APA use is associated with retained but reduced benefit from enalapril.
Angiotensin-Converting Enzyme Inhibitors↗
Acute haemodynamic effects of the beta 1-adrenoceptor partial agonist xamoterol at rest and during supine exercise in patients with left ventricular dysfunction due to ischaemic heart disease: a double-blind randomized trial.
The effects of xamoterol 0.2 mg kg-1 i.v. and placebo on left ventricular function at rest and on exercise were compared in patients with left ventricular dysfunction due to ischaemic heart disease. Improvements were seen in systolic and diastolic function at rest, and at up to 50% of maximal exercise, without evidence of worsening myocardial ischaemia.
Adrenergic beta-Agonists↗
Influence of autonomic neuropathy upon left ventricular dysfunction in insulin-dependent diabetic patients.
BACKGROUND: Diabetic cardiomyopathy is a well-defined complication of diabetes that occurs in the absence of ischemic, vascular, and hypertensive disease. HYPOTHESIS: The study was undertaken to test the relationship among autonomic neuropathy (AN), 24-h blood pressure (BP) profile, and left ventricular function. METHODS: Nineteen type-1 diabetic patients underwent autonomic tests and echocardiographic examination. Patients were divided according to the presence (AN+) or absence (AN-) of AN. RESULTS: In the AN+ group (n = 8), the E/A ratio at echo was lower than in the AN- group (n = 11) (1.1 +/- 0.3 vs. 1.6 +/- 0.3; p < 0.005). Systolic and diastolic BP reductions during sleep were smaller in the AN+ than in the AN- group (6.6 +/- 6.6 vs. 13.0 +/- 4.3%; p < 0.03 for systolic and 12.8 +/- 6.8 vs. 20.0 +/- 4.0% for diastolic BP reduction; p < 0.03, respectively). Considering all patients, the E/A ratio correlated inversely with awake diastolic BP (r - 0.63; p = 0.005); sleep systolic BP (r - 0.48; p = 0.04), and sleep diastolic BP (r - 0.67; p = 0.002). The AN correlated with diastolic interventricular septum thickness (r 0.57; p = 0.01), sleep systolic BP (r 0.45; p = 0.05), sleep diastolic BP (r 0.54; p = 0.02), and correlated inversely with systolic and diastolic sleep BP reduction (r - 0.49; p = 0.03 and r - 0.67; p = 0.002, respectively). Finally, E/A ratio and AN score correlated between themselves (r - 0.6; p = 0.005). CONCLUSION: Our results suggest that left ventricular diastolic dysfunction may be detected very early in type-1 diabetic patients with AN. Parasympathetic lesion and nocturnal elevations in BP could be the link between AN and diastolic ventricular dysfunction.
Adult↗
No evidence for systolic or diastolic left ventricular dysfunction at rest in selected patients with long-term type I diabetes mellitus.
We assessed left ventricular systolic and diastolic function using pulsed-waved Doppler echocardiography in a selected group of 20 patients with insulin-dependent diabetes mellitus (IDDM) (mean age, 35 +/- 8 years; mean diabetes duration, 17 + 7 years). Our patients were free of autonomic neuropathy and major micro- or macrovascular complications and had no evidence of ischemic heart disease or hypertension. The results were compared with those of 20 age- and sex-matched control subjects. We found that left ventricular geometry and mass, systolic function by M-mode and 2D-echocardiography, isovolumetric relaxation time, deceleration time and the PEP/LVET ratio were not significantly different between patients and control subjects. Hemodynamic parameters were also not significantly different except for a slightly higher heart rate in the patient group (75 +/- 11 vs. 68 + 6 bpm, P = 0.019). After correction of A-peak velocities for differences in heart rate, there was no significant difference of Doppler indices of diastolic left ventricular function between patients and control subjects. The absence of significant left ventricular systolic and diastolic dysfunction by Doppler echocardiography in our study patients may be explained by our patient selection. Left ventricular dysfunction in diabetic patients without concomitant hypertensive or ischemic heart disease may only occur in conjunction with microvascular disease in other organ systems, with autonomic neuropathy or with poor metabolic control.
Adult↗
Improved survival for stenting vs. balloon angioplasty for the treatment of coronary artery disease in patients with ischemic left ventricular dysfunction.
While earlier studies of balloon angioplasty (BA) in patients with left ventricular (LV) dysfunction suggested high late mortality, a study directly comparing coronary stenting and BA has not been performed. Since stenting provides a more durable revascularization, we sought to compare long-term survival in patients undergoing stenting vs BA in patients with decreased left ventricular ejection fractions (LVEF). We evaluated consecutive patient procedures performed in our institution from 1996 through 1999. Patients were considered part of the stent group if they received at least one stent. To be included, patients had to have a technically adequate angiographic LV gram with a calculated LVEF<or=50%. Patients with prior CABG were excluded. Mortality data was retrieved using the United States Social Security Death Index. Follow-up ranged from 3.5 to 6.5 years. Statistical analysis was performed and tests were significant with a P-value<0.05. A total of 238 patients fulfilled our criteria. Mean age was 57.5+/-12 years, mean LVEF was 39+/-10%, 67% were males, 71.5% received stents, 62% had a recent MI, and 19% died during follow-up. Overall 5-year survival was 84% for stenting and 77% for BA (P=NS). Patients with an LVEF<or=40% (n=110) had better survival at 5 years if they received a stent compared with BA alone (76% for stents vs. 53% for BA; P<0.05). Stenting was found to be significant predictor of late survival on Cox Hazard Regression analysis in patients with an LVEF<or=50% and LVEF<or=40%. This study demonstrates improved 5-year survival for patients undergoing stenting compared with balloon angioplasty in patients with LVEF<or=40%.
Angioplasty, Balloon, Coronary↗
Left ventricular dysfunction after acute myocardial infarction: results of a prospective multicenter study.
In a multicenter prospective study of 866 patients who survived the coronary care unit phase of an acute myocardial infarction, variables reflecting left ventricular function were examined to assess their impact on 2 year survival. Single variables that reflected left ventricular dysfunction before infarction and in the acute and recovery phases were, respectively, history of prior myocardial infarction, rales in the coronary care unit dichotomized at greater than bibasilar and predischarge radionuclide ejection fraction dichotomized at less than 0.40. When combined in a stepwise fashion, patients lacking these three risk characteristics had a 2 year 4.2% mortality rate, whereas patients possessing all three characteristics had a 45% mortality rate. Rales in the coronary care unit and predischarge ejection fraction act independently, and each contributes to mortality. Fifty-two patients with advanced rales but an ejection fraction of 0.40 or greater had a 21% mortality rate. Similarly, 208 patients with few rales but an ejection fraction of less than 0.40 had a 15% mortality rate. These data suggest that the mortality risk imposed by those factors that assess permanent left ventricular damage is independent of and additive to the mortality risk contributed by dynamic, acute phase dysfunction. These data fit the hypothesis that acute phase dysfunction is, in part, due to transient ischemia that, on reversal, can restore function toward normal. The results suggest 1) that assessment of left ventricular function during the acute and recovery phases of myocardial infarction is necessary to define prognostic characteristics of an individual patient, and 2) that of particular importance is the identification of patients whose postinfarction course is consistent with reversible ischemia.
Cardiac Output↗