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We compared the short-term hemodynamic effects of isosorbide dinitrate (40 mg orally) and captopril (25 mg orally) in 18 patients with severe chronic heart failure in a randomized, crossover study conducted on consecutive days. Captopril and isosorbide dinitrate produced similar decreases in systemic vascular resistance, but whereas nitrate therapy decreased pulmonary arteriolar resistance significantly, captopril did not; the difference between the two drugs was highly significant (-25% vs -5%, p less than 0.001). Left ventricular filling pressures declined similarly with both captopril (-10.5 mm Hg) and with isosorbide dinitrate (-9.3 mm Hg), but because pulmonary arteriolar resistance fell significantly with nitrate therapy, mean right atrial pressure decreased more with isosorbide dinitrate than with captopril (-5.4 vs -2.8 mm Hg, respectively; p less than 0.001). Although systemic resistance declined similarly with both drugs, cardiac index increased more with nitrate therapy than during converting-enzyme inhibition (+0.47 vs +0.23 L/min/m2) (p less than 0.01), and therefore mean arterial pressure fell less with isosorbide dinitrate than with captopril (-10.5 mm Hg vs -16.7 mm Hg); p less than 0.05); two patients developed symptomatic hypotension with captopril, whereas none did so with the nitrate. The difference in the effects of the two drugs on cardiac index was not due to differences in their effects on heart rate, since heart rate fell similarly with both drugs, and thus both drugs produced similar increases in stroke volume index. These data indicate that, in patients with severe chronic heart failure, nitrates exert favorable dilating effects on the pulmonary circulation not shared by captopril.(ABSTRACT TRUNCATED AT 250 WORDS)
Left ventricular dysfunction has been suggested as a cause of late potentials on the signal averaged ECG of patients with coronary artery disease. We compared the averaged surface ECG with angiographic findings in 57 patients with coronary artery disease and left ventricular dysfunction. Sixteen patients had sustained ventricular tachycardia and 41 had no documented arrhythmia. These two patient groups were comparable with respect to age, mean ejection fraction, and wall motion score. Late potentials, defined as voltage less than 25 microV in the last 40 msec of the filtered QRS complex, were found in 10 of 16 patients with ventricular tachycardia and in 6 of 41 patients without arrhythmia (p less than 0.005). However, late potentials were independent of ejection fraction, wall motion score, or presence of dyskinesis in both groups. There was no correlation between the total filtered QRS duration and ejection fraction or wall motion score in either patient group. In patients with coronary artery disease, late potentials are associated with ventricular tachycardia but are independent of global or regional left ventricular function. This finding has important implications for studies of the prognostic value of late potentials following myocardial infarction.
We used blood pool radionuclide angiography to study the left ventricular (LV) ejection fraction (EF) in 17 patients with a centrifugal assist device (AD) placed because of severe postoperative LV dysfunction. During maximal LVAD flow, the 12 patients who could be weaned had a higher LV-EF than the 5 who could not be weaned (18 +/- 12% vs. 9 +/- 2%, p = 0.04). Sequential studies during variable AD flows in 12 patients revealed an increase in LV-EF from 15 +/- 7% at maximal flows to 33 +/- 8% during minimal flows (p less than 0.005) in the 10 patients who could be weaned and no change in LV-EF in 2 patients who could not be weaned. The LV-EF during maximal LVAD flow rates was similar in the 10 patients with long-term survival (192 +/- 129 days) and in the 7 patients with only short-term (9 +/- 6 days) survival (LV-EF 17 +/- 12% vs. 12 +/- 6%, p = ns). The long-term survivors, however, had a substantial increase in LV-EF from 20 +/- 13% to 34 +/- 9% (p less than 0.01), as the LVAD flow was decreased from maximal to minimal, whereas the short-term survivors had an insignificant increase in LV-EF from 12 +/- 7% to 21 +/- 12% (p = ns). The long-term survivors increased the LV-EF from maximal to minimal LVAD flows by 182%, in contrast with the short-term survivors, who increased the LV-EF by only 44%.(ABSTRACT TRUNCATED AT 250 WORDS)
PURPOSE: To analyze the follow-up of left ventricular function (LVF) after surgical correction of severe chronic aortic insufficiency (AI). METHODS: Twenty-one out of 68 patients with AI, initially asymptomatic and that developed symptoms during the follow-up period of 24-36 months, were studied. Relationship between symptoms and LVF by echocardiogram and radioisotopic ventriculography at rest and in isotonic exercise were studied. Three clinical moments (CM) were assumed: CM-0- at the beginning of the study, when all patients were asymptomatic; CM-1- manifestation of the symptoms during 24-36 months; CM-2- corresponding to the late post-operative period of 8 months of 20 out of 21 patients (one refused the surgery). The analysis did not show any significant differences between the mean values of all echocardiographic variables (diastolic and systolic diameters, shortening fraction, final systolic stress, volume-mass ratio, contractility index) and the ejection fraction of the left ventricle (EF) obtained by the radioisotope ventriculography at rest and, including exercise, between clinical moments 0 and 1. RESULTS: In the CM-2, involution was verified for functional class I/II in all cases and absence of expressive complications or immediate or late postoperative mortality. Comparison between CM-2 and 0 showed expressive regression of the diameters at rest in the postoperative period and with significant improvement in the means mainly the percentual variation of the EF and total time of effort. CONCLUSION: Symptoms assembled patients with more advanced eccentric hypertrophy and did not coincide with any immediate change in findings studied at rest and at exercise. It represented a point of reference for surgical indication compatible with late postoperative involution of chronic adaptation of AI.
In order to determine the relationship of the peak systolic pressure/end-systolic volume (PSP/ESV) ratio to standard ejection phase indices [ejection fraction (EF), mean normalized systolic ejection rate (MNSER), mean velocity of circumferential fiber shortening (Vcf)], and ventricular function curves (VFC), hemodynamic and angiographic studies were carried out in 38 subjects: 11 normal controls (Group I) and 27 with coronary artery disease (CAD). The CAD patients were subdivided into those without (Group II) and those with (Group III) regional asynergy. EF, MNSER and Vcf were calculated from the ventriculogram using standard formulae. The slope of the left ventricular function curve was constructed by determining left ventricular stroke work index and left ventricular end-diastolic pressure before and after ventriculography, and dividing the change in the left ventricular stroke work index by the change in the left ventricular end-diastolic pressure. Peak systolic left ventricular pressure was determined before left ventriculography; minimal systolic volume was measured from the left ventriculogram. PSP/ESV ratio in the control group (Group I) was 6.4 +/- 2.8. This differed significantly from the ratio in patients (Group II) with CAD but without asynergy (4.7 +/- 2.2 p less than 0.025) and from that in patients (Group III) with CAD and asynergy (2.4 +/- 1.4, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
We were able to diagnose right ventricular infarction (RVI) by transesophageal echocardiography (TEE) in a patient with acute inferior infarction, and it was confirmed by cardiac catheterization. To evaluate right ventricular (RV) function quantitatively, area shortening (AS) and regional AS (rAS) were measured from RV images obtained by TEE. The AS correlated with RV ejection fraction obtained by radionuclide angiography (r = 0.72). The patient with RVI showed depressed RV function by AS measurement with decreased rASs of all regions in the acute phase. In the chronic phase, RV function of the patient improved, especially in the region of the ventricular septum and apex regions. These results indicate availability of TEE and that RV function can be evaluated by TEE.
To assess the utility of double oblique, ECG-gated 1H magnetic resonance (MR) derived volume curves for assessing LV function, cardiac short axis images were acquired with a fast field echo technique. We applied this methodology to assess left ventricular function in three groups: normals, patients with left ventricular hypertrophy, and dilated cardiomyopathy. Six slices with 16-20 phases per RR interval were analyzed, representing the initial 75-80% of the cardiac cycle. For each slice, the endocardial border of the left ventricular (LV) chamber was manually traced. Using Simpson's rule, the total LV volume at a given phase was determined considering the traced area, thickness and position in three-dimensional space of each of the six constituent slices. The calculated volumes were plotted against time and the stroke volume, ejection fraction and cardiac output were determined. The volume vs time plots for the systolic and diastolic portions of the curve were individually fit to third degree polynomials using a least squares approximation. From the fit curves, the following data were extracted: the mean slope (dV/dT) during filling and emptying, and the time to 1/4, 1/3 and 1/2 filling and emptying. These parameters are valuable indices of the functional status of the myocardium; thus, accurate and useful estimates of LV function can be obtained using MRI derived volume curves in normal and abnormal states.
Clinical data, function and compliance of left ventricle as well as regional wall motion were analysed in 17 patients with preoperatively limited left-ventricular function and signs of myocardial ischaemia after complete revascularisation surgery. Recatheterisation after 5.2 months on average after surgery showed improvement by one NYHA class, an increase of mean left-ventricular enddiastolic pressure, which was interpreted as "improved status of ischaemia", a decrease of left-ventricular compliance by 30%, of enddiastolic volume by 14% and of endsystolic volume by 20% (P less than 0.05). Loss of function occurred in 3 out of 92 bypasses. Up to the time of reporting, 22.4 months postoperatively, all patients have survived in a relatively satisfactory clinical state. All parameters of left-ventricular function as well as regional wall motion showed a tendency for improvement after surgery in the majority of patients. However, pre- and postoperative mean values were not significantly different (P greater than 0.05). Thus, despite clearcut improvement of clinical state and "ischaemia index", improvement of left-ventricular function and regional wall motion are not consistently demonstrable. The reasons of this discrepancy cannot be ascertained by this investigation. The quality of the surgical intervention and the sensitivity of parameter assessment cannot be held responsible.
Left ventricular systolic dysfunction related to ventricular arrhythmias is a relatively poorly understood entity. To increase our knowledge base, we describe 5 patients in whom the link between ventricular dysfunction and ventricular arrhythmia was unequivocally established. All patients had repetitive monomorphic ventricular arrhythmias and left ventricular systolic dysfunction (ejection fraction < or =40% and end-diastolic size > or =55 mm). The arrhythmogenic source was identified by electrophysiological study (right ventricle in 2 patients, left ventricle in 2, and left sinus of Valsalva in one), and was eliminated in all patients by radiofrequency catheter ablation. At 7+/-2 months post-ablation, large improvements were seen in left ventricular function and remodeling (ejection fraction >/=50% and end-diastolic size < or =51 mm in all cases), with no recurrence of arrhythmia during follow-up (10-69 months). This finding confirms that recurring ventricular arrhythmias can induce left ventricular dysfunction which may be reversible after ablation.
OBJECTIVE: Patients with ischemic heart failure may benefit from coronary artery bypass grafting. The histopathological variables associated with improvement in ejection fraction 6 months after surgery were assessed. METHODS: This study comprised 24 patients indicated for coronary artery bypass grafting, ejection fraction < 35%, functional class II-IV heart failure, and mean age 59 +/- 9 years. Endomyocardial biopsies were performed during and 6 months after surgery. Extension of the fibrosis, number of cells with myocytolysis, and hypertrophy of the muscle fiber were quantified by using a system of image analysis. Clinical and functional review was repeated within 6 months. RESULTS: A significant improvement in heart failure functional class was observed in 16 patients after 6 months of follow-up (from NYHA functional class 2.8 +/- 0.7 to 1.7 +/- 0.6; P < 0.001), but the ejection fraction did not change (25 +/- 6 % vs. 26 +/- 10%). Hypertrophy of the muscle fiber was similar in the specimens biopsied in the pre- and postoperative periods (21 +/- 4 vs. 22 +/- 4 microm), but the extension of fibrosis (8 +/- 8 vs. 21 +/- 15% area) and the number of cells with myocytolysis (9 +/- 11 vs. 21 +/- 15% cell) significantly increased. However, the composition of a histological score combining those 3 variables indicated a greater increase in the ventricular function of those with a lower degree of preoperative histopathological alterations. CONCLUSION: Patients with ischemic cardiomyopathy undergoing coronary artery bypass grafting improved their ventricular function when the preoperative adverse histopathological alterations were of a lower degree.
Serial changes in cardiac function after surgery were studied in 84 patients with various valvular heart diseases using M-mode and two-dimensional echocardiography (2-DE). The results were as follows: 1. Serial postoperative changes in cardiac dimensions and left ventricular functions were well documented by M-mode and 2-DE. 2. The change in left ventricular function became most pronounced one month after surgery, and remained unchanged in many patients during the subsequent observation periods. 3. Open mitral commissurotomy (OMC) and mitral valve replacement (MVR) were compared as to their benefits for patients with isolated mitral stenosis (MS) accompanied by left ventricular dysfunction, and MVR proved superior to OMC in terms of magnitude of functional improvement. 4. (a) Ejection fraction (EF) in patients with left ventricular volume overload was overestimated due to the influence of increased preload. Accordingly, EF which tended to be depressed one month after surgery was judged to reflect altered loading conditions; it did not represent myocardial damage caused by valve replacement. (b) In patients who had MVR or aortic valve replacement (AVR) without postoperative heart failure, EF remained unchanged in the MVR group after a lapse of one month postoperatively, while it tended to improve in the AVR group. This difference was thought to be caused by changes in left ventricular systolic overload resulting from correction of regurgitation. (c) In patients with MR and postoperative heart failure, there was a tendency for EF to decrease after a lapse of one month postoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)
The incidence of ischemic ECG-changes and anginal symptoms during PTCA and the influence of PTCA on left ventricular function were studied in a consecutive series of 40 patients with recanalized infarct artery and significant (greater than 50%) single vessel disease. PTCA was performed within the first week (4.1 +/- 2.5 days) after intravenous streptokinase (1.5 Mio U i.v. over 60 min) in acute myocardial infarction (duration of pain less than four hours). The primary success rate of PTCA was 78% (31/40). In 25 of 31 (81%) successfully dilated patients, there were ischemic ECG-changes (ST-segment elevation greater than 0.1 mV), and in 14 patients anginal symptoms were observed during balloon inflation. Follow-up angiography after six months showed restenosis or reocclusion in 5/22 (23%) of the patients with an ischemic reaction, and in 3/6 (50%) without ischemic signs during PTCA. Only patients with an ischemic reaction and without restenosis demonstrated an increase in left ventricular ejection fraction (p less than 0.05) and regional wall motion in the infarct region (p less than 0.01), in contrast to patients with restenosis or without an ischemic reaction during angioplasty. Thus, after intravenous streptokinase an ischemic reaction can be detected in a high percentage (81%) as an indicator of salvaged myocardium. Significant improvement of left ventricular function was only demonstrable in patients with ischemic signs during PTCA without restenosis.
The purpose of this study was to analyze long-term follow-up information from patients treated with stenting for unprotected left main coronary artery (LMCA) stenosis. Stenting of unprotected LMCA stenosis is often performed in selected patients, but the long-term safety of this therapy is not yet established. Between January 1995 and September 2000, 270 consecutive patients with unprotected LMCA stenosis and normal left ventricular function who underwent treatment at 4 clinical centers were included in this study. Data were forwarded to the coordinating center using a standard case report form. The procedural success rate was 98.9%. There were no deaths, 3 stent thromboses, and 3 Q-wave myocardial infarctions during the hospitalization. Angiographic follow-up was performed in 237 patients (follow-up rate 87.8%), and the restenosis rate was 21.1%. The reference size was an independent predictor of binary restenosis (odds ratio 0.543, 95% confidence interval 0.308 to 0.957, p = 0.03). During the follow-up period (32.3 +/- 18.5 months), there were 20 deaths (8 cardiac, 12 noncardiac) and 5 nonfatal myocardial infarctions. Target and new lesion revascularizations were required in 45 (16.7%) and 31 (11.5%) patients, respectively. The cumulative probabilities free from major adverse cardiac events were 81.9 +/- 2.4%, 78.4 +/- 2.6%, and 77.7 +/- 2.7%, respectively, at 1, 2, and 3 years. Combined coronary artery disease and postprocedural minimal luminal diameter were the significant predictors of major adverse cardiac events. Thus, the long-term prognosis of patients after stenting of unprotected LMCA stenosis was favorable in selected patients with normal left ventricular function.
OBJECTIVES: This study evaluated the effects of oral therapy with coenzyme Q on echocardiographic and hemodynamic indexes of left ventricular function and on quality of life in patients with chronic left ventricular dysfunction. BACKGROUND: Coenzyme Q is a coenzyme for oxidative phosphorylation and an antioxidant and free radical scavenger. It has been claimed to improve symptoms, quality of life, left ventricular ejection fraction and prognosis in patients with cardiac failure. METHODS: Thirty patients with ischemic or idiopathic dilated cardiomyopathy and chronic left ventricular dysfunction (ejection fraction 26 +/- 6%) were randomized to a double-blind crossover trial of oral coenzyme Q versus placebo, each for 3 months. Right heart pressures, cardiac output and echocardiographic left ventricular volumes were measured at baseline and after each treatment phase, and quality of life was assessed using the Minnesota "Living With Heart Failure" questionnaire. It was calculated that to demonstrate an increase in left ventricular ejection fraction from 25% to 30% with a standard deviation of 5% using 95% confidence intervals with a power of 80% we would require 17 patients. RESULTS: Twenty-seven completed both treatment phases. There was no significant difference in left ventricular ejection fraction, cardiac volumes or hemodynamic and quality of life indices after treatment with coenzyme Q or placebo, although plasma coenzyme Q levels increased from 903 +/- 345 nmol/l(-1) to 2,029 +/- 856 nmol/l(-1). CONCLUSIONS: In patients with left ventricular dysfunction, treatment for three months with oral coenzyme Q failed to improve resting left ventricular systolic function or quality of life despite an increase in plasma levels of coenzyme Q to more than twice basal values.
Experimental myocardial infarction of the posterolateral wall of the left ventricle was produced in dogs by injecting 80 micron microspheres into the left circumflex coronary artery to determine changes in regional myocardial function after infarction, to examine how the changes in regional myocardial function relate to the changes in global left ventricular function, and to examine the relationship between regional wall motion and wall thickening after myocardial infarction. Serial measurements of global ventricular and regional myocardial function were made in six dogs before and during 20 days after infarction, with the use of M-mode echocardiography and chronic Swan-Ganz catheter implantation. One hour after infarction, stroke volume index had decreased 49% from baseline, percent fractional shortening had decreased 52%, lateral wall motion had decreased 80%, and lateral wall thickening had decreased 100%. By 6 days after infarction, stroke volume index had increased 41% from its low point, percent fractional shortening had increased 34%, and lateral wall motion had increased 100% toward but not to baseline. Lateral wall thickening did not return following infarction. Peak and end-systolic circumferential wall stresses and systemic arterial blood pressure remained stable. End-systolic diameter increased acutely (36%) after infarction and did not change during the 20-day time period, while end-diastolic diameter gradually increased, resulting in the increase in percent fractional shortening. In conclusion, after posterolateral wall infarction, wall motion can return without an improvement in regional myocardial function, presumably because the infarcted region stiffens, allowing it to be pulled inward.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND AND OBJECTIVE: Left ventricular function is the most important predictor of survival in patients with coronary artery disease. It is also an important indicator for hospital mortality after operation for end-stage coronary artery disease. In our study we investigated, how preoperative ventricular dysfunction influences long term survival after coronary bypass surgery. PATIENTS AND METHODS: Between 4/1986 and 12/2000, 1751 patients (1440 men/311 women) with left ventricular ejection fraction (LVEF) 10-30% underwent coronary bypass grafting (CABG) at the Deutsches Herzzentrum Berlin. The age of the patients was calculated to an average of 59,2 years. The prime criterion for CABG was ischemia ("hibernating myocardium") diagnosed by myocardial scintigraphy, echocardiography and in some cases with magnetic resonance imaging and positron emission tomography. RESULTS: Operative mortality for the group was 7,1%. The actuarial survival rate was 87,6% after 2 years, 76,0% after 5, and 53,3% after 9. 455 had LVEF 10-20%, in these actuarial survival was 79,8% after 2 years, 63,0% after 5 and 45,7% after 9 years. CONCLUSION: We conclude that CABG can be used successfully to improve life expectancy of patients with end-stage coronary artery disease. CABG leads to acceptable prognosis for these high-risk patients when the myocardium is preoperatively identified as being viable.
We determined the relationship between myocardial infarct size (MIS) estimated by electrocardiographic measurements of infarct size (QRS score) and left ventricular function estimated by angiographically left ventricular ejection fraction (EF). MIS estimated by QRS score were the same in both DM and NDM (5.2 +/- 0.5 vs 4.3 +/- 0.4: p greater than 0.05), but EF in DM was significantly lower than in NDM (43.1 +/- 1.4 vs 51. +/- 1.1%: p less than 0.05). There was clear linear correlation between MIS and EF in NDM (r = -0.71) but not in DM. EF was much lower in DM than in NDM even at the same QRS score level. There were no differences in blood pressure, serum lipid levels, age, and the site of the myocardial infarction. The most likely explanation for this appears to be due to a previous left ventricular disease in DM.