Background and purpose: To estimate healthcare resource utilization among patients with heart failure (HF) with preserved (HFpEF) versus reduced (HFrEF) ejection fraction using population data from ...

Aim: The aim of this study was to assess the impact of long‐term physical training on left ventricular longitudinal contraction by strain rate analysis and tissue tracking imaging.

BackgroundCardiac resynchronization reduces symptoms and improves left ventricular function in many patients with heart failure due to left ventricular systolic dysfunction and cardiac dyssynchrony. We evaluated its effects on morbidity and mortality.MethodsPatients with New York Heart Association class III or IV heart failure due to left ventricular systolic dysfunction and cardiac dyssynchrony who were receiving standard pharmacologic therapy were randomly assigned to receive medical therapy alone or with cardiac resynchronization. The primary end point was the time to death from any cause or an unplanned hospitalization for a major cardiovascular event. The principal secondary end point was death from any cause.ResultsA total of 813 patients were enrolled and followed for a mean of 29.4 months. The primary end point was reached by 159 patients in the cardiac-resynchronization group, as compared with 224 patients in the medical-therapy group (39 percent vs. 55 percent; hazard ratio, 0.63; 95 percent confidence interval, 0.51 to 0.77; P<0.001). There were 82 deaths in the cardiac-resynchronization group, as compared with 120 in the medical-therapy group (20 percent vs. 30 percent; hazard ratio 0.64; 95 percent confidence interval, 0.48 to 0.85; P<0.002). As compared with medical therapy, cardiac resynchronization reduced the interventricular mechanical delay, the end-systolic volume index, and the area of the mitral regurgitant jet; increased the left ventricular ejection fraction; and improved symptoms and the quality of life (P<0.01 for all comparisons).ConclusionsIn patients with heart failure and cardiac dyssynchrony, cardiac resynchronization improves symptoms and the quality of life and reduces complications and the risk of death. These benefits are in addition to those afforded by standard pharmacologic therapy. The implantation of a cardiac-resynchronization device should routinely be considered in such patients.

The prognostic value of repeated echocardiographic measurement of left ventricular function after acute myocardial infarction was evaluated. We found that repeated measurements of wall motion index in survivors of acute myocardial infarction, with no reinfarction, provide important prognostic information about death and worsening of heart failure.

Following an acute myocardial infarction (AMI) there is immediate deterioration of contractility in the infarcted left ventricular (LV) wall. This can be followed by regional dilation (expansion) as well as global remodeling. We examined 35 consecutive patients--with no history of myocardial ischemia--who were admitted to hospital within 3 hours after initial symptoms and with ST-segment changes on an electrocardiogram consistent with transmural ischemia. Echocardiography was performed at admission, and at 6 hours, 12 hours, 24 hours, 3 days, and 6 days after onset of the AMI. Within 3 hours after onset of symptoms an increase in both end-diastolic volume index (EDVI) and end-systolic volume index (ESVI) was found in both anterior and inferior infarcts when compared with healthy controls (mean +/- SD EDVI: 99 +/- 13 ml/m2 [anterior], 69 +/- 17 ml/m2 [inferior], 51 +/- 15 ml/m2 [controls], p < or = 0.00001; ESVI: 62 +/- 12 ml/m2 [anterior], 38 +/- 11 ml/m2 [inferior], 17 +/- 6 ml/m2 [controls], p < or = 0.00001). At all points in time, volumes were larger in anterior infarcts than in inferior infarcts (p < 0.05). The volumes did not change during the 6 days (p > 0.1). Thus, major LV dilation is present within 3 hours after onset of symptoms of first AMI. The dilation is more pronounced in anterior versus inferior infarcts. From 3 hours until day 6 no further changes in LV volumes occurred.

To elucidate a possible antiarrhythmic effect of long-chained n-3 polyunsaturated fatty acids, heart rate variability was assessed in 52 patients with a previous myocardial infarction and left ventricular dysfunction. The content of n-3 polyunsaturated fatty acids in platelets was closely associated with the patient's fish-consuming habits, and a significant positive correlation was observed between the n-3 fatty acid docosahexaenoic acid and heart rate variability.

There is evidence for an antiarrhythmic effect of n-3 polyunsaturated fatty acids (n-3 PUFA) in animals. The aim of the present study was to investigate the effect of dietary n-3 PUFA on ventricular arrhythmias and heart rate variability (HRV) in patients with a previous myocardial infarction. Fifty-five patients were randomized to receive either 5.2 g of n-3 PUFA daily for 12 weeks or placebo in a double blind, placebo-controlled study. Prior to randomization a 24-hour Holter recording was obtained, and this was repeated at the end of the study. The major end-points were the number of ventricular extrasystoles (VE)/24 hours and the 24-hour HRV. A non-significant decrease in VE/24 hours was found in both the n-3 PUFA group and among controls after dietary supplementation, whereas HRV significantly increased after n-3 PUFA compared to both baseline values (p = 0.04) and to controls (p = 0.01). The present study therefore supports the hypothesis that n-3 PUFA may have an anti-arrhythmic effect in humans.

Marine n-3 polyunsaturated fatty acids may protect against ischaemic heart disease.1 In the diet and reinfarction trial patients with an acute myocardial infarction advised to eat fish rich in n-3 polyunsaturated fatty acids had a 29% reduction in two year all cause mortality compared with controls.2 The authors hypothesised that dietary n-3 polyunsaturated fatty acids might reduce malignant ventricular arrhythmias and sudden cardiac death, as reported in animals.3 We investigated a possible antiarrhythmic effect of dietary n-3 polyunsaturated fatty acids in survivors of myocardial infarction. Patients were eligible for study if they had been discharged from the department of cardiology at Aalborg Hospital between November 1991 and August 1993 after a myocardial infarction and had a ventricular ejection fraction below 0.40. We excluded patients aged over 75, patients with pacemakers or permanent tachyarrhythmias, and those with serious non-cardiac disease. Eighty one patients fulfilled the inclusion criteria and 55 gave informed consent to a double blind placebo controlled trial. Patients were randomly …

The aim of this study was to assess the importance of congestive heart failure and left ventricular (LV) systolic dysfunction after an acute myocardial infarction (AMI) on long-term mortality in different age groups. A total of 7,001 consecutive enzyme-confirmed AMIs (6,676 patients) were screened for entry into the TRAndolapril Cardiac Evaluation (TRACE) study. Medical history, echocardiographic estimation of LV systolic function determined as wall motion index, infarct complications, and survival were documented for all patients. To study the importance of congestive heart failure and wall motion index independent of age, we performed Cox proportional-hazard models in 4 different age strata (≤55 years, 56 to 65 years, 66 to 75 years, and >75 years). Patients in these strata had 1 -year mortality rates of 5%, 11%, 21%, and 32%, respectively. Three-year mortality rates were 11%, 20%, 34%, and 55%, respectively. The risk ratios (and 95% confidence limits) associated with congestive heart failure in the same 4 age strata were 1.9 (1.3 to 2.9), 2.8 (2.1 to 3.7), 1.8 (1.5 to 2.2) and 1.8 (1.5 to 2.2), respectively. The risk ratios associated with decreasing wall motion index were 6.5 (3.6 to 11.4), 3.3 (2.3 to 4.6), 2.7 (2.2 to 3.4), and 2.1 (1.7 to 2.6), respectively. In absolute percentages, there was an excess 3-year mortality associated with congestive heart failure in the 4 age strata of 14%, 24%, 25%, and 28%, respectively. The absolute excess in 3-year mortality associated with LV systolic dysfunction in the 4 age strata was 15%, 19%, 25%, and 21%, respectively. Thus, the relative importance of LV systolic dysfunction and congestive heart failure diminished with increasing age. However, the absolute excess mortality associated with congestive heart failure and LV systolic dysfunction was more pronounced in the elderly than in the young.

The relationship between plasma ANP and systolic and diastolic left ventricular myocardial function, as determined by echocardiography, was investigated. Thirty-one patients were examined 24 h after onset of acute myocardial infarction. The systolic parameters measured were: wall motion index (WMI), ejection fraction, systolic volume index and diastolic volume index. Diastolic function was evaluated by mitral flow analysis and isovolumic relaxation time. The following parameters were measured in the mitral flow: peak velocity of early flow, peak velocity of atrial flow, the earlylatrial ratio, deceleration rate of the early flow and atrial filling fraction. A blood sample was drawn from each patient for ANP analysis at the same time as the echocardiographic examination. A correlation between plasma-ANP and systolic function was found (ejection fraction: r = -0.60, P < 0.001; systolic volume index: r = 0.68, P < 0.001; diastolic volume index: r = 0.47, P < 0.01; WMI: r = -0.42, P < 0.05) whereas no correlation was found between any of the diastolic parameters and plasma ANP (P > 0.10 for all the variables). We conclude that there is a significant correlation between plasma ANP and systolic function, as evaluated by echocardiography 24 h after AMI, whereas there was no corresponding relationship between plasma ANP and diastolic function.

The relationship between plasma ANP and systolic and diastolic left ventricular myocardial function, as determined by echocardiography, was investigated. Thirty-one patients were examined 24 h after onset of acute myocardial infarction. The systolic parameters measured were: wall motion index (WMI), ejection fraction, systolic volume index and diastolic volume index. Diastolic function was evaluated by mitral flow analysis and isovolumic relaxation time. The following parameters were measured in the mitral flow: peak velocity of early flow, peak velocity of atrial flow, the earlylatrial ratio, deceleration rate of the early flow and atrial filling fraction. A blood sample was drawn from each patient for ANP analysis at the same time as the echocardiographic examination. A correlation between plasma-ANP and systolic function was found (ejection fraction: r = -0.60, P < 0.001; systolic volume index: r = 0.68, P < 0.001; diastolic volume index: r = 0.47, P < 0.01; WMI: r = -0.42, P < 0.05) whereas no correlation was found between any of the diastolic parameters and plasma ANP (P > 0.10 for all the variables). We conclude that there is a significant correlation between plasma ANP and systolic function, as evaluated by echocardiography 24 h after AMI, whereas there was no corresponding relationship between plasma ANP and diastolic function.

The TRAndolapril Cardiac Evaluation (TRACE) study is evaluating the effect of angiotensin-converting enzyme inhibition with trandolapril on mortality (overall and cardiovascular) and cardiovascular morbidity in patients surviving myocardial infarction (MI) with reduced left ventricular (LV) function. TRACE is a randomized, double-blind, placebo controlled study conducted in 27 centers in Denmark. Eligible patients had a MI verified by elevated cardiac enzymes, electrocardiographic changes, and/or chest pain as well as reduced LV function, as shown by electrocardiographic evaluation of wall motion index less than or equal to 1.2. (A wall motion index less than or equal to 1.2 approximates to a left ventricular ejection fraction less than or equal to 35%.) Patients with residual ischemia and/or heart failure were not excluded. Trandolapril or placebo was added to conventional therapy 3-7 days after MI. Between May 1990 and June 1992, 6,674 patients (7,010 infarctions) were screened. A total of 2,614 patients had a wall motion index less than or equal to 1.2; of these, 1,749 were included. Overall 1-year mortality of the patients entered into the study was 24%. Treatment will be continued for 2-4 years (mean, 3 years), ending In mid 1994. The design and organization of the study, the outcome of screening, and demographic features of the screened population are described.

In clinical practice there is a need for a method to measure pulmonary congestion in left sided heart failure. Current methods, including auscultation and chest X-rays, are imprecise, semiquantitative, and assess fluid accumulation, not impairment of lung function. This paper evaluates the use of a mathematical model of pulmonary gas exchange as a measure of pulmonary congestion in left sided heart failure. Eleven patients with pulmonary congestion were investigated on admission and during anticongestive therapy. Inspired oxygen fraction was varied, and measurements of ventilation and blood gasses were used to estimate model parameters i.e. pulmonary shunt and ventillation-perfusion (V/Q) mismatch (DeltaPO2). On admission, patients' parameters were: shunt, median 9.9 % (range 0.0 - 22.2 %), and DeltaPO2, 4.3 kPa (range 1.8 - 6.1 kPa), values outside the range of normal subjects (shunt, median 1.2 % range 0.0 - 11.1 %, DeltaPO2, median 0.1 kPa range 0.0 - 2.0 kPa) (p < 0.001). During therapy both shunt and V/Q mismatch were reduced (shunt, median 7.8 % range 3.7 -14.4 %, DeltaPO2, median 2.8 kPa range 0.2 - 3.9 kPa). This study illustrates a possible role for gas exchange parameters to quantify pulmonary congestion in patients with left-sided heart failure, and to monitor the effect of therapy.*