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Effects of the angiotensin converting enzyme inhibitor enalapril on the long-term progression of left ventricular dysfunction in patients with heart failure. SOLVD Investigators.

BACKGROUND: In patients with heart failure, activation of the renin-angiotensin system is common and has been postulated to provide a stimulus for further left ventricular (LV) structural and functional derangement. We tested the hypothesis that chronic administration of the angiotensin converting enzyme (ACE) inhibitor enalapril prevents or reverses LV dilatation and systolic dysfunction among patients with depressed ejection fraction (EF) and symptomatic heart failure. METHODS AND RESULTS: We examined subsets of patients enrolled in the Treatment Trial of Studies of Left Ventricular Dysfunction (SOLVD). Fifty-six patients with mild to moderate heart failure underwent serial radionuclide ventriculograms, and 16 underwent serial left heart catheterizations, before and after randomization to enalapril (2.5-20 mg/day) or placebo. At 1 year, there were significant treatment differences in LV end-diastolic volume (EDV; p less than 0.01), end-systolic volume (ESV; p less than 0.005), and EF (p less than 0.05). These effects resulted from increases in EDV (mean +/- SD, 136 +/- 27 to 151 +/- 38 ml/m2) and ESV (103 +/- 24 to 116 +/- 24 ml/m2) in the placebo group and decreases in EDV (140 +/- 44 to 127 +/- 37 ml/m2) and ESV (106 +/- 42 to 93 +/- 37 ml/m2) in the enalapril group. Mean LVEF increased in enalapril patients from 0.25 +/- 0.07 to 0.29 +/- 0.08 (p less than 0.01). There was a significant treatment difference in LV end-diastolic pressure at 1 year (p less than 0.05), with changes paralleling those of EDV. The time constant of LV relaxation changed only in the placebo group (p less than 0.01 versus enalapril), increasing from 59.2 +/- 8.0 to 67.8 +/- 7.2 msec. Serial radionuclide studies over a period of 33 months showed increases in LV volumes only in the placebo group. Two weeks after withdrawal of enalapril, EDV and ESV increased to baseline levels but not to the higher levels observed with placebo. CONCLUSIONS: In patients with heart failure and reduced LVEF, chronic ACE inhibition with enalapril prevents progressive LV dilatation and systolic dysfunction (increased ESV). These effects probably result from a combination of altered remodeling and sustained reduction in preload and afterload.

Angiotensin-Converting Enzyme Inhibitors↗

Indications for immediate angiotensin-converting enzyme inhibition in patients with acute myocardial infarction.

When initiated a few days after myocardial infarction, angiotensin-converting enzyme inhibition exerts beneficial effects on survival and morbidity in patients with asymptomatic left ventricular systolic dysfunction or symptomatic heart failure. During the acute phase of a myocardial infarction, angiotensin-converting enzyme inhibition appears to be well tolerated, to prevent the development of heart failure in patients with asymptomatic left ventricular systolic dysfunction and to improve the hemodynamic and clinical variables of heart failure when present. Accordingly, early angiotensin-converting enzyme inhibition is clearly indicated in patients with acute myocardial infarction associated with asymptomatic left ventricular dysfunction or clinical evidence of heart failure. Angiotensin-converting enzyme inhibition may also be beneficial when thrombolytic agents fail to restore coronary patency in patients with acute myocardial infarction.

Angiotensin-Converting Enzyme Inhibitors↗

Predictive power of ejection fraction and renal failure in patients admitted for chest pain without ST elevation in the troponin era.

BACKGROUND: Ejection fraction (EF) and renal failure (RF) are powerful predictors of mortality in patients with myocardial infarction (MI). There are limited data assessing the predictive value of EF and RF compared with clinical variables in patients without ST elevation using troponin as the diagnostic MI criteria. METHODS: Consecutive patients admitted from the emergency department underwent serial assessment of cardiac markers, including troponin I. Abnormal EF was defined as < 50%; RF, as creatinine clearance (CrCl) < 60 mL/min. Multivariate analysis was used to compare clinical variables, CrCl, and EF for predicting short- and long-term outcomes. RESULTS: A total of 3074 patients had EF assessed. Mild to moderately reduced EF and CrCl were present in 639 (21%) and 582 (19%) patients, with 403 (13%) and 233 (7.6%) having severe systolic dysfunction and severe RF, respectively. Abnormal EF and RF were both present in 13% of patients (1-year mortality 26%), whereas 52% had both normal EF and CrCl (1-year mortality 3.2%). The presence of either systolic dysfunction or RF increased mortality 3- to 4-fold compared with patients without either. The most important multivariate predictors of 1-year mortality were EF (OR 2.6 [95% CI 1.7-3.8, P < .0001]) and CrCl (OR 2.8 [95% CI 1.8-4.2, P < .0001]). CONCLUSIONS: Both RF and EF are strong predictors of cardiac mortality in patients admitted for exclusion of MI. Prediction models that do not include these 2 variables will underestimate risk.

Aged↗

Effect of antecedent systemic hypertension on subsequent left ventricular dilation after acute myocardial infarction (from the Survival and Ventricular Enlargement trial).

Whether antecedent systemic hypertension influences the risk of subsequent left ventricular (LV) dilation in patients after an acute myocardial infarction with LV systolic dysfunction is unclear. We assessed echocardiographic evidence of ventricular remodeling from baseline (mean +/- SD 11 +/- 3 days) to 2 years after an acute myocardial infarction in 122 hypertensive (defined as a history of treated hypertension, baseline systolic blood pressure > or =140 or baseline diastolic blood pressure > or =90 mm Hg) and 334 nonhypertensive patients in the Survival and Ventricular Enlargement echocardiographic substudy. Compared with nonhypertensives, baseline heart size, defined as the sum of the average short- and long-axis LV cavity areas, was similar (70.1 +/- 11.9 vs 68.8 +/- 11.2 cm(2), p = 0.33 at end-diastole; 50.1 +/- 11.3 vs 48.8 +/- 10.8 cm(2), p = 0.31 at end-systole), but short-axis LV myocardial area (24.7 +/- 4.3 vs 25.7 +/- 5.0 cm(2), p = 0.043) and wall thickness (1.15 +/- 0.16 vs 1.21 +/- 0.17 cm, p = 0.004) at end-diastole were greater among hypertensives. The myocardial infarct segment lengths were similar in the 2 groups (p = 0.22). Although LV cavity areas increased significantly in the 2 groups from baseline to 2 years (p < or =0.001), the increase was significantly greater in hypertensives than in nonhypertensives (+5.6 +/- 11.5 vs +2.2 +/- 10.7 cm(2), p = 0.005 at end-diastole; +6.23 +/- 12.75 vs +2.94 +/- 11.4 cm(2), p = 0.012 at end-systole). There was no concomitant difference in the change in LV myocardial area or LV wall thickness between the 2 groups (p >0.30). After adjusting for known confounders, antecedent hypertension was associated with a doubling of the risk of LV dilation (50.8% vs 37.7%, odds ratio 2.09, 95% confidence interval 1.27 to 3.45, p = 0.004). This association was not modified by diabetes mellitus, myocardial infarct segment length, or captopril use (all p values for interaction >0.10). We conclude that antecedent hypertension is associated with subsequent LV dilation in patients after acute myocardial infarction with LV systolic dysfunction.

Antihypertensive Agents↗

Effect of obesity and being overweight on long-term mortality in congestive heart failure: influence of left ventricular systolic function.

AIMS: Previous studies have suggested that a high body mass index (BMI) is associated with an improved outcome in congestive heart failure (CHF). However, the studies addressing this problem have not included enough patients with non-systolic heart failure to evaluate how left ventricular systolic function interacts with obesity on prognosis in CHF. The aim of this study was to evaluate how BMI influences mortality in patients hospitalized with CHF, and to address in particular whether the effect of BMI is influenced by left ventricular (LV) systolic function. METHODS AND RESULTS: Retrospective analysis of baseline and survival data for 4700 hospitalized CHF patients for whom BMI was available. LV systolic function, as assessed by wall motion index was available for 95% of the patients. Follow-up time ranged from 5 to 8 years. In the total population, the risk of death decreased steadily with increasing BMI from the underweight to the obese. Compared with normal weight, and adjusted for sex and age, risk ratios (RR) and 95% confidence limits were: underweight 1.56 (1.33-1.84), overweight 0.90 (0.83-0.97), obese 0.77 (0.70-0.86). Being underweight conferred a greater risk in CHF patients with normal systolic function [RR 1.66 (1.29-2.14), compared with normal weight] than in patients with reduced systolic function [RR 1.11 (0.87-1.42), P for interaction 0.03]. In patients with systolic dysfunction, obesity was associated with increased risk compared with normal weight [RR 1.21 (1.01-1.45)]. CONCLUSION: Increasing BMI in CHF is associated with a lower mortality, but the influence is complex and depends on left ventricular systolic function. Hence, in patients with systolic dysfunction obesity may indicate an increased risk.

Aged↗

Diastolic hibernation masquerading as constrictive pericarditis.

BACKGROUND: Hibernating myocardium has traditionally been characterized in terms of systolic dysfunction. METHODS: We describe a case in which a 75-year-old patient with significant coronary artery disease was operated upon for classic constrictive pericarditis. RESULTS: At sternotomy, there was no evidence of pericarditis, but marked diastolic without systolic dysfunction remained. After successful coronary revascularization, the patient immediately exhibited dramatic improvement of diastolic performance. Ex vivo evaluation of myocardial contractile function revealed normal myocardial adrenergic responsiveness, indicating a reversible impairment of contractility. CONCLUSION: Diastolic hibernation may therefore represent a unique form of surgically correctable restrictive cardiomyopathy.

Aged↗

[Prognosis of diastolic cardiac insufficiency].

The natural history and prognosis of diastolic cardiac failure are difficult to determine because of the large differences in the studies which have been performed in this field. The ten studies published to date concerning the prognosis have been performed on hospital populations and, consequently, only the most severe cases have been recruited. Moreover, the threshold values of indices of the ejection phase used to define systolic dysfunction vary from one study to another. A review of these papers provides a rather disconcerting appreciation of the annual mortality rate (from 1.3% to 17.5%). The differences in aetiology, age and threshold values of parameters of systolic function probably explain most of the variability observed. Taking unbiased studies alone in consideration, such as the Framingham study, the mean annual mortality of diastolic cardiac failure between 55 and 71 years, is 3 to 9%, much less than that observed with predominantly systolic dysfunction (15 to 20%). Other prospective studies, adjusting morbidity and mortality to age and other principal prognostic factors, are awaited.

Cardiac Output, Low↗

[Clinical and prognostic significance of disturbed global and regional contractility of left ventricle in diphtheria myocarditis].

Examination of 159 diphtheria patients diagnosed myocarditis in 64 of them. The latter were divided into 3 groups: with mild, moderate and severe myocarditis. The patients with and without diphtheria have undergone two-dimensional echocardiography with estimation of the asinergia index (AI) and left ventricular (LV) ejection fraction. Pronounced systolic dysfunction was revealed only in severe diphtheric myocarditis (DM). AI rose in moderate and severe DM. By the degree of AI elevation it can be judged about myocarditis severity and the disease prognosis. Regional LV contractility and LV systolic dysfunction were correlated. A group of patients with severe DM was identified who had a high risk of death in akinesia of LV segments (IA > 2) and lowering of LV ejection fraction below 35%.

Adult↗

Effects of anaemia on cardiovascular status.

Cardiomyopathy is a common, heterogeneous and important cause of cardiac morbidity and mortality in uraemic patients. The risks of ischaemic heart disease, cardiac failure, and death increase progressively from lowest risk in patients with concentric left-ventricular hypertrophy, to medium risk in patients with left-ventricular dilatation but intact systolic function, to highest risk in patients with systolic dysfunction. Anaemia and hypertension are the reversible risk factors most consistently linked with the development of cardiomyopathy in these patients. Longitudinal data show that anaemia predisposes individuals to initial left ventricular dilatation, with compensatory hypertrophy, which may progress to systolic dysfunction. This process typically begins at glomerular filtration rates between 25 and 50 ml/min, and haemoglobin concentrations that are even slightly below normal are associated with progressive cardiac enlargement. Several observational studies have suggested that the correction of anaemia may reduce mortality and hospitalization rates in dialysis patients. The available evidence supports maintaining haemoglobin concentrations to greater than 11 g/dl. Whether a haemoglobin threshold exists above which no further benefit is seen remains controversial, partially because recent randomized controlled trials have intervened relatively late in the anaemia cardiomyopathy cardiac failure death continuum. One large randomized controlled trial showed no benefit from normalizing the haemoglobin concentration in haemodialysis patients with well-established cardiac disease; however, these patients had been exposed to anaemia for long periods of time and were at the extreme end of the cardiorenal disease spectrum. Other researchers have demonstrated a protective effect of normalizing the haemoglobin concentration in patients with asymptomatic, and hence presumably early, cardiomyopathy. The psychological benefits and improvements in exercise tolerance and quality of life resulting from normalization of the haemoglobin concentration are becoming clearer. However, conclusive evidence of the cardiovascular benefits of earlier, more aggressive treatment of renal anaemia as well as of the exact target haemoglobin concentration at which risk begins to develop is still lacking. The results of ongoing trials should help to clarify both of these issues within the next 5 years.

Anemia↗

[Dilated cardiomyopathy: recent advances and current treatment].

The combination of dilatation and systolic dysfunction of the left or both ventricles from idiopathic or specific origin define dilated cardiomyopathy (DC). It is an important cause of cardiac morbidity through congestive heart failure (CHF) or arrhythmias. Prevalence studies estimate a rate of left ventricular systolic dysfunction of 2% to 3% or more, and of 1.5% of CHF among the general population. Genetic studies on familial DC have identified at least 5 genetic locus. In addition, the role of virus, genetic abnormalities, immunologic responses and increased myocardial apoptosis are factors recognized factors that play a significant role in the pathogenesis of idiopathic DC. Mortality in severe CHF may reach 50% at 2 years after diagnosis. The introduction of "triple" therapy combining diuretics, digoxin and angiotensin converting enzyme inhibitors (ACEI) has significantly decreased this high mortality. Recent large, multicentric clinical trials on drugs aimed to diminish the neuroendocrine hyperactivity of patients in stable chronic CHF (betablockers and spirolactone) have resulted in an additional reduction in total mortality of about 35% in relation with control groups. Betablockers, compared to ACEI, also diminish the rate of sudden death prompting their almost mandatory indication in the absence of contraindications. Cardiac transplantation presently offers a survival rate of 66% at 5 years but donor scarcity has stabilized the number of procedures. In patients resuscitated from malignant arrhytmias the implantation of defibrillators offers a better survival than drugs. Future advances in the knowledge of the pathogenesis and especially of genetic mechanisms, may substantially change the understanding and treatment of these disorders.

Cardiomyopathy, Dilated↗

Identification of viable myocardium in patients with chronic coronary artery disease and left ventricular dysfunction: role of magnetic resonance imaging.

Nineteen patients (16 men and 3 women, mean age 51 years) with previous anterior myocardial infarction and severe stenosis (> or = 90%) of the left anterior descending coronary artery were studied by magnetic resonance imaging (MRI) without and with contrast media to verify the capability of MRI in identifying viable myocardium in areas of severe systolic dysfunction. In corresponding left ventricular segments, a comparison was made between regional signal intensities (SI) determined on MRI images before and 4, 8, 12, and 30 minutes after administration of paramagnetic contrast media (gadolinium diethylenetriaminepentaacetic acid, 0.4 mmol/kg intravenously) and metabolic parameters determined by iodine 123 phenylpentadecanoic acid (IPPA) scintigraphy. The SI and the time of maximum postcontrast enhancement were analyzed by dividing the left ventricle into 11 segments. Each segment was classified as normal (group 1, n = 116), hibernating (group 2, n = 50), or necrotic (group 3, n = 43) on the basis of the IPPA washout rate (> 30%, 10% to 30%, and < 10%, respectively). Regional SI demonstrated significant differences in absolute values at 12 minutes (group 3: 1.62 +/- 0.58 vs group 1: 1.32 +/- 0.52, p < 0.01, and vs group 2: 1.34 +/- 0.48, p < 0.05) and at 30 minutes (group 3: 1.71 +/- 0.47 vs group 1: 1.21 +/- 0.55, p < 0.01, and vs group 2: 1.49 +/- 0.57, p < 0.05) and in temporal distribution. These results suggest that MRI has a potential role in differentiating viable from necrotic myocardium in patients with chronic severe systolic dysfunction.

Contrast Media↗

Prognostic impact of peak oxygen uptake and percentage of predicted value of peak oxygen uptake in patients with left ventricular dysfunction.

BACKGROUND: Comparing the prognostic value of peak oxygen uptake (VO2max) in absolute values and percentage of predicted VO2max (%PredVO2) in terms of prognostic stratification, contradictory references are found in the medical literature. In theory, the measurement of VO2max relative to a normal subject should improve its predictive capacity, because VO2max is influenced by gender, weight, physical activity and age. OBJECTIVES: To compare the prognostic value of VO2max and %PredVO2 (Jones equation) in an adult population (> or = 20 years) of patients with left ventricular systolic dysfunction and to study the influence of age on these parameters. POPULATION AND METHODS: We review data from the first cardiopulmonary stress test performed in 295 consecutive patients with left ventricular systolic dysfunction (ejection fraction < or = 40%); mean age was 52 +/- 10 years, 81% were male, and 76 aged > or = 60 years. In 52%, the etiology was ischemic. We evaluated demographic and clinical variables, the baseline ECG and the medication used before the test. We compared VO2max (ml/kg/min) and %PredVO2 in terms of prognostic stratification for the combined endpoint (death and/or heart transplant) for 2 years of follow-up. RESULTS: We detected 60 patients with events (42 deaths and 18 transplants). ROC curve analysis was used to determine the best cut-off value for VO2max and %PredVO2 to identify patients with events. The best cut-off for VO2max was < or = 19 ml/kg/min and < or = 49% for %PredVO2 in the total population, and in the event-free survival analysis, by log-rank test, we obtained p < 0.001 for both cut-offs. Considering the two extreme age groups (20-40 years and > or = 60 years), we found different cut-off values. In the youngest group we obtained VO2max of < or = 23 ml/kg/min and %PredVO2 of < or = 59%, and in the elderly < or = 12.5 ml/kg/min and < or = 64% respectively. For the intermediate group, the cut-off values were the same as for the total population. In the youngest patients, the new cut-offs did not offer an improvement in accuracy. In the elderly, for VO2max, we obtained an improvement in specificity from 28 to 86% and a reduction in sensitivity from 95 to 50%, with an improvement in accuracy from 46.8 to 75.9% (p = 0.05). With regard to %PredVO2, specificity fell from 86 to 61% and sensitivity increased from 50 to 82%, with similar accuracy (75.9 to 67%, p = 0.78). CONCLUSIONS: In the extreme age groups, we obtained different cut-off values, but only for the elderly (VO2max < or = 12.5 ml/kg/min and %PredVO2 < or = 64%). A benefit in terms of accuracy was only obtained in respect of VO2max, because for %PredVO2, there is already a correction for age through the Jones equation.

Adult↗

The CARE-HF study (CArdiac REsynchronisation in Heart Failure study): rationale, design and end-points.

BACKGROUND: Cardiac resynchronisation is a promising new intervention for patients with heart failure, left ventricular systolic dysfunction and ventricular dyssynchrony. OBJECTIVE: The CARE-HF trial is designed to evaluate the long-term effects of cardiac (atrio-bi-ventricular) resynchronisation on the mortality and morbidity of patients with heart failure due to left ventricular systolic dysfunction already receiving diuretics and optimal medical therapy with ACE inhibitors and beta-blockers (where indicated and tolerated). METHODS AND RESULTS: Approximately 800 patients will be randomised to device therapy or control and followed for a minimum of 18 months. A pragmatic study design has been chosen that does not attempt to conceal allocation from investigators or patients because it is impossible to guarantee maintenance of blinding for the duration of the study. The end-points committee will adjudicate events in a blinded fashion. Since cardiac resynchronisation may alter other aspects of the management of the patient, as would occur in clinical practice, the study should be considered a comparison of strategies rather than simply of a device. The primary end-point is all-cause mortality or unplanned cardiovascular hospitalisation. The study should complete recruitment during 2002 and report in 2004.

Adrenergic beta-Antagonists↗

Abnormalities of left ventricular filling in patients with coronary artery disease: assessment by colour M-mode Doppler technique.

In 54 healthy individuals and 107 patients with coronary artery disease, intraventricular early filling velocities were recorded by colour M-mode Doppler. The time difference between the occurrence of peak velocity in the apical region and at the mitral tip was calculated, and normalized by dividing it by the mitral to apical distance. Transmitral velocities were determined by the single pulsed Doppler technique. The patients were divided into groups according to systolic function as assessed by left ventriculography. The normalized time difference was similar in the reference group (12 +/- 8 ms.cm-1) and the patient group with no electrocardiographical signs of previous infarction and normal ventriculography (16 +/- 16 ms.cm-1). It increased significantly in the group with infarction and/or regional systolic dysfunction (43 +/- 21 ms.cm-1), and a further increase was present in the group with severely impaired ventricles (53 +/- 14 ms.cm-1). The ratio between peak early and late transmitral velocity fell significantly in the group with infarction and/or regional systolic dysfunction, but was normalized in the group with severely impaired ventricles. Colour M-mode Doppler shows that apical filling is delayed in patients with injured left ventricles due to coronary artery disease. This delay increases with progression of ventricular injury. The technique may be an important addition to transmitral pulsed Doppler in assessing left ventricular filling.

Adult↗

Comparing methods to identify general internal medicine clinic patients with chronic heart failure.

OBJECTIVES: Identification of patients with left ventricular systolic dysfunction is the first step in identifying which patients may benefit from clinical practice guidelines. The purpose of this study was to develop and validate a computerized tool using clinical information that is commonly available to identify patients with left ventricular systolic dysfunction (LVSD). METHODS: We performed a cross-sectional study of patients seen in a Department of Veterans Affairs General Internal Medicine Clinic who had echocardiography or radionuclide ventriculography performed as part of their clinical care. RESULTS: We identified 2246 subjects who had at least one cardiac imaging study. A total of 778 (34.6%) subjects met study criteria for LVSD. Subjects with LVSD were slightly older than subjects without LVSD (70 years vs 68 years, P =.00002) but were similar with regard to sex and race. Subjects with LVSD were more likely to have prescriptions for angiotensin-converting enzyme (ACE) inhibitors, carvedilol, digoxin, loop diuretics, hydralazine, nitrates, and angiotensin II receptor antagonists. Of the variables included in the final predictive model, ACE inhibitors, loop diuretics, and digoxin exerted the greatest predictive power. Discriminant analysis demonstrated that models containing pharmacy information were consistently more accurate (75% accurate [65% sensitivity, 81% specificity]) than those models that contained only International Classification of Diseases, 9th revision (ICD-9), codes, including ICD-9 codes for congestive heart failure (72% accurate [80% sensitivity, 68% specificity]). CONCLUSIONS: We demonstrated that an automated, computer-driven algorithm identifying LVSD permits simple, rapid, and timely identification of patients with congestive heart failure by use of only routinely collected data. Future research is needed to develop accurate electronic identification of heart failure and other common chronic conditions.

Aged↗

Cardiac resynchronization therapy for congestive heart failure.

Cardiac resynchronization represents a novel therapeutic strategy for the treatment of congestive heart failure due to systolic dysfunction. Since its modest beginnings in the 1990s, cardiac resynchronization therapy has gained widespread acceptance as a useful adjunct to pharmacologic therapy for congestive heart failure. Randomized trials have consistently shown functional improvement in patients with congestive heart failure due to systolic dysfunction, a wide QRS complex on electrocardiogram and sinus rhythm, that are treated with cardiac resynchronization therapy. This review article will address the rationale, mechanisms of action, limitations and appropriate selection of patients for cardiac resynchronization therapy.

Cardiac Pacing, Artificial↗

Nitroprusside in critically ill patients with left ventricular dysfunction and aortic stenosis.

BACKGROUND: Vasodilators are considered to be contraindicated in patients with severe aortic stenosis because of concern that they may precipitate life-threatening hypotension. However, vasodilators such as nitroprusside may improve myocardial performance if peripheral vasoconstriction is contributing to afterload. METHODS: We determined the response to intravenous nitroprusside in 25 patients with severe aortic stenosis and left ventricular systolic dysfunction. Patients were included in the study if they had been admitted to the intensive care unit for invasive hemodynamic monitoring of heart failure and if they had a depressed ejection fraction (<or=0.35), severe aortic stenosis (aortic-valve area, <or=1 cm2), and a depressed cardiac index (<or=2.2 liters per minute per square meter). Patients were excluded if they had hypotension, defined as either the need for intravenous inotropic or pressor agents or a low mean systemic arterial pressure (<60 mm Hg). Patients were enrolled irrespective of other, coexisting valve disease or coronary artery disease. RESULTS: At base line, the mean (+/-SD) ejection fraction was 0.21+/-0.08; the aortic-valve area was 0.6+/-0.2 cm2, with peak and mean gradients of 65+/-37 and 39+/-23 mm Hg, respectively; and the cardiac index was 1.60+/-0.35 liters per minute per square meter. After six hours of therapy with nitroprusside (at which time the dose had been increased to a mean of 103+/-67 microg per minute), the cardiac index had increased to 2.22+/-0.44 liters per minute per square meter (P<0.001 for the comparison with base line). After 24 hours of nitroprusside infusion (dose, 128+/-96 microg per minute), the cardiac index had increased further, to 2.52+/-0.55 liters per minute per square meter (P<0.001 for the comparison with base line). Nitroprusside was well tolerated and had minimal side effects. CONCLUSIONS: Nitroprusside rapidly and markedly improves cardiac function in patients with decompensated heart failure due to severe left ventricular systolic dysfunction and severe aortic stenosis. It provides a safe and effective bridge to aortic-valve replacement or oral vasodilator therapy in these critically ill patients.

Aged↗

Relation of T-wave alternans to regional left ventricular dysfunction and eccentric hypertrophy secondary to coronary heart disease.

Left ventricular (LV) hypertrophy and structural disease are associated with exaggerated repolarization dispersion and risk for cardiac arrest. We hypothesized that T-wave alternans (TWA) from the electrocardiogram, reflecting proarrhythmic repolarization dispersion, would increase with extent of eccentric LV hypertrophy and vary spatially with the distribution of myocardial scar. We studied 28 patients with coronary disease, systolic dysfunction, and nonsustained ventricular tachycardia. On echocardiography, 21 patients had wall motion abnormalities and 20 had LV hypertrophy (mass index > or =100 g/m(2)). TWA magnitude (voltage of alternation), which was computed spectrally during ventricular stimulation, varied linearly with LV mass index (p = 0.003). Spatially, positive TWA (magnitude > or =1.9 microV) in orthogonal electrocardiographic axes overlaid scar or wall motion abnormalities in corresponding echocardiographic segments (p <0.05 in x and y axes). After a follow-up of 35 +/- 13 months, positive TWA predicted the combined end point of death or sustained ventricular arrhythmias in all patients (p = 0.025), with a trend for those with echocardiographic LV hypertrophy (p = 0.058). In conclusion, in patients with systolic dysfunction due to coronary artery disease, TWA may indicate arrhythmic contributions from regional myocardial scar and eccentric LV hypertrophy.

Aged↗