Echocardiographic assessment of left ventricular hypertrophy.
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Biomedical subjects
Publications and source records attributed to N Reichek.
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A technique for epicardial mapping of segmental myocardial function at multiple sites over both right and left ventricles was developed using a high-resolution, 7.5-MHz, short-focus, miniaturized, M-mode echocardiographic transducer worn on the fingertip. Myocardial function was determined from the extent and time course of systolic thickening and diastolic thinning at each site mapped. The technique was characterized in an open-chest canine model of myocardial ischemia. Ischemia was induced by transient or permanent coronary occlusion in 17 dogs. Acute occlusions produced reduced segmental thickening within 10-15 seconds and, often, overt systolic thinning of ischemic myocardium. Rhodamine fluorescence perfusion maps were compared with echocardiographic maps in nine dogs. Segmental thickening was reduced in perfused segments adjacent to, but not involved by, ischemia, as well as ischemic segments. Reproducibility appeared satisfactory for quantitative analysis of grouped data on multiple segments, and qualitative analysis in individual segments. Initial human studies performed during coronary bypass surgery in 11 subjects showed echocardiographic abnormalities in the six patients with ventriculographic abnormalities and in four with normal ventriculograms. Transmural infarctions were akinetic, showing no change in thickness throughout the cardiac cycle. Hypokinetic segments distal to high-grade coronary stenosis were common, although most segments distal to stenosis contracted normally. Reversal of segmental contraction abnormalities by coronary bypass grafting was shown in three subjects, while worsening of function was seen in previously abnormal segments in two and in a previously normal segment in one subject. Epicardial echocardiographic mapping is a practical method for intraoperative assessment of myocardial function during coronary surgery in man that may enhance our understanding of the pathophysiology of coronary disease and the effects of coronary surgery.
Pirbuterol (PB), an oral beta-adrenergic-receptor agonist, has the pharmacologic effects of vasodilation and positive inotropy. The present studies were undertaken to determine the value of PB in the long-term therapy of chronic cardiac failure. A double-blind, randomized, 7-week trial comparing PB (20 mg three times daily) with placebo in 12 patients was followed by 12 weeks of open PB therapy. Dose-dependent nervousness and tremulousness limited the unit PB dose to less than 20 mg in six patients. In all patients, clinical status, exercise tolerance and maximal oxygen uptake, left ventricular echocardiographic dimension and cardiothoracic ratio were unchanged from control after 7 weeks of placebo or PB or after 12--19 weeks of PB. To assess the adequacy of 20 mg of PB, the dose-response relations of cardiocirculatory effects to 10, 15, 20 and 30 mg of PB were compared in seven of the above patients and nine other patients. Cardiac output was significantly elevated and wedge pressure reduced after all four doses, but these changes were sustained from 6 hours after 20- and 30-mg doses only. Thus, the role of PB in the management of chronic cardiac failure appears limited; judgment of its utility must await the results of additional controlled trials.
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Catheter sepsis remains a persistent, though infrequent, complication of intravenous hyperalimentation (IVH). Those select patients requiring home hyperalimentation delivered through Silastic catheters are subject to this serious problem. Reported in this article is a case of Enterococcus endocarditis of the tricuspid valve in a patient receiving home IVH; the endocarditis was recognized early using two-dimensional echocardiography and was treated successfully with catheter removal and IV antibiotic administration. Ideal conditions exist for the formation of endocarditis in the setting of catheter sepsis with parenteral nutrition. Routine echocardiography is indicated when catheter sepsis is documented, since early diagnosis and treatment may reduce invasive cardiac tissue infection and permanent injury. The right atrial catheter generates reflections during echocardiography that require special attention for accurate interpretation.
We examined the relationship between echocardiographic and hemodynamic parameters in 48 patients with left ventricular ejection fractions less than 50% without primary valvular disease. Pulmonary wedge pressure (PWP) correlated with the PR-AC interval (r = -0.62) and with left atrial dimension (r = 0.64) but not with left ventricular diastolic dimension. A PR-AC interval less than or equal to 60 msec was observed in 26 of 29 (90%) patients with a PWP greater than or equal to 14 mm Hg versus 1 of 10 (10%) patients with a PWP less than 14 mm Hg. The correlation between PWP and the PR-AC interval was substantially better in patients with a PR interval less than or equal to 200 msec (r = -0.79) than in patients with a PR interval greater than 200 msec (r = -0.55). The PR-AC interval also correlated with the ejection fraction (r = 0.47). A left atrial dimension greater than or equal to 4.0 cm was observed in 29 of 35 (83%) patients with a PWP greater than or equal to 14 mm Hg versus 0 of 9 (0%) patients with a PWP less than 14 mm Hg. Stroke volume (SV) correlated with aortic root excursion (r = 0.71) and with SV calculated from formulas based on mitral valve motion (r = 0.76) or aortic valve motion (r = 0.62). However, no echo formula provided valid estimates of cardiac output. We conclude that M-mode echocardiography provides a relatively useful noninvasive method of assessing left ventricular filling pressure in patients with reduced ejection fraction and no valvular disease.
To determine the reliability of two dimensional echographic images of the left ventricle with different two dimensional echographic instruments, two dimensional echographic images of the left ventricle were compared in vitro using two phased array and two mechanical systems to image 22 short axis slices of the three postmortem human hearts (one with infarction, one with left ventricular aneurysm, one with mitral regurgitation). Total left ventricular area and left ventricular cavity area were determined with planimetry and myocardial area was derived by subtraction. Comparison of total, myocardial and cavity areas with calibrated photographs of each slice showed excellent correlations for each echographic system (r = 0.93 to 0.97 for total area; 0.90 to 0.94 for cavity area; 0.89 to 0.95 for myocardial area). For total left ventricular area, the ratio of echographic to photographic image size was close to unity (0.95 to 1.08) for one mechanical and two phased array systems, but significantly lower for mechanical system 2 (0.71, p less than 0.001). For myocardial area the echographic/photographic ratio was also close to unity (0.96 to 1.15) for two phase array systems and mechanical system 1 but significantly lower for mechanical system 2 (0.77, p less than 0.005). In contrast, all systems underestimated left ventricular cavity area with lower, more variable echographic/photographic ratios (0.48 to 0.78), with mechanical system 2 again giving significantly lower values (p less than 0.02) than the other systems. Underestimation of left ventricular cavity area appears to result from inaccurate endocardial display. We conclude that accurate left ventricular image quantitation is possible with either phased array or mechanical systems if each variable studied is calibrated against an independent reference standard and echographic results are corrected by the resultant regression equation.
To determine the effect of diuresis on the performance of the failing left ventricle, we measured cardiac output, pulmonary wedge pressure and M-mode echo left ventricular diastolic dimension before and after diuresis in 13 patients with heart failure. Diuresis increased stroke volume (43 +/- 23 ml to 50 +/- 18 ml (p less than 0.05)) and decreased pulmonary wedge pressure (28 +/- 3 mm Hg to 19 +/- 5 mm Hg (p less than 0.01)), mean blood pressure (100 +/- 14 mm Hg to 88 +/- 10 mm Hg (p less than 0.01)) and systemic vascular resistance (2,059 +/- 622 dynes-sec-cm-5 to 1,783 +/- 556 dynes-sec-cm-5 (p less than 0.05)). Echo left ventricular diastolic dimension was not changed by diuresis (6.0 +/- 0.8 cm to 6.0 +/- 0.8 cm). Percent change in stroke volume correlated with systemic vascular resistance (r = 0.60, p less than 0.05) and with left ventricular diastolic dimension (r = 0.62, p less than 0.05) but not with pulmonary wedge pressure (r = 0.12) or right atrial pressure (r = 0.04). Thus, diuresis improved the performance of the failing ventricle and reduced afterload, but it did not alter left ventricular diastolic dimension, an index of preload. These data suggest that diuresis improves ventricular function by decreasing afterload.
Anatomic, echocardiographic and ECG findings of left ventricular hypertrophy (LVH) were compared in 34 subjects. Echocardiographic LV mass correlated weel with postmortem LV weight (r = 0.96) and accurately diagnosed LVH (sensitivity 93%, specificity 95%). In contrast, Romhilt-Estes (RE) point score and Sokolow-Lyon (SL) voltage criteria for ECG LVH were insensitive (50% and 21%, respectively) but specific (both 95%). RE correlated weakly with LV weight (r = 0.64), but SL did not. Echocardiographic LV mass was then compared with RE and SL in an unselected clinical series of 100 subjects, in 28 subjects with severe aortic stenosis (AS) and in 14 with severe aortic regurgitation (AR). Results in the clinical series were comparable to those in the necropsy series. In the AS and AR groups, with a high prevalence of LVH, the low sensitivity of RE point score and Sl criteria led to poor overall results. Analysis of individual ECG variables showed that most voltage information is contained in leads aVL and V1. Correction of voltage for distance from the left ventricle did not substantially improve results. Individual nonvoltage criteria were each nearly as sensitive as RE point score. We could not devise new ECG criteria that improved diagnostic results. We conclude that the ECG is specific but insensitive in recognition of LVH. Moreover, when true LVH prevalence is less than 10%, more false-positive than true-positive diagnoses will be obtained. M-mode echocardiographic LV mass is superior to ECG criteria for clinical diagnosis of LVH.
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A pedicled diaphragmatic skeletal muscle graft was used to replace a portion of resected right ventricle in 35 dogs. The graft contracted when electrically stimulated directly or via the phrenic nerve before and after insertion. The electrical pacing threshold was lower for phrenic nerve stimulation (0.9 +/- 0.20 mamp) than for direct graft stimulation (2.3 +/- 1.19 mamp). The heart could be captured and paced by stimulating the muscle graft with higher current (16.2 +/- 4.49 mamp). The delay from pacing stimulus to muscle graft contraction when the graft was paced directly was 10 msec. The epicardial activation time delay when the heart was paced through the muscle graft was 27.0 +/- 9.08 msec. When the muscle graft pedicle was transected, the graft lost its ability to contract. The heart, however, could still be captured electrically through the graft for up to 4 hours. Strain gauge studies of the nonstimulated muscle graft showed tension development during pre-ejection ventricular contraction identical to that of the right ventricle. In the ejection phase, muscle graft tension slowly declined. The stimulated muscle graft developed active tension and echographically demonstrated muscle thickening during contraction. This study demonstrates that a vascularized, neurally innervated diaphragmatic muscle graft can be placed into the right ventricle. The graft retains its ability to contract in response to direct or phrenic nerve stimulation. It can be made to contract during any phase of the cardiac cycle. Thus diaphragmatic muscle grafts may provide a method to augment ventricular cavity size with synchronously contracting muscle.
Patients with cardiac failure have a generalized sympathetic vasoconstriction that may impair cardiac function and exercise tolerance. The ability of long-term alpha-receptor blockade and vasodilation with trimazosin (TMZ) to improve exercise capacity was studied in patients with chronic, stable heart failure of varying severity (functional exercise classes B to D). Exercise performance was monitored by respiratory gas exchange and air flow before and after patients were randomized to placebo (13 patients) or TMZ were then followed on treatment for up to 52 weeks. Significant (P less than 0.05) and sustained increases in exercise capacity, oxygen uptake, and oxygen pulse were observed with TMZ treatment in each Class B or C patient and in six of nine Class D patients, and were not observed during treatment with placebo.
We report clinical experience with the coronary vasodilator nifedipine in 127 patients with symptoms of myocardial ischemia associated with electrocardiographic or angiographic evidence, or both, of coronary-artery spasm. In the majority of patients conventional antianginal therapy including nitrates and beta-adrenergic blockers failed, and in one third of the patients at least one episode of ventricular tachycardia developed during an attack of angina. Nifedipine (40 to 160 mg every 24 hours) significantly reduced the mean weekly rate of anginal attacks from 16 to two (P less than 0.001). Similar marked reductions in the nitroglycerin requirement were noted. In 63 per cent of the patients complete control of anginal attacks was achieved, and in 87 per cent the frequency of angina was reduced by at least 50 per cent. Nifedipine was generally well tolerated, with only 5 per cent of the patients requiring termination of the drug because of intolerable side effects. This experience with nifedipine suggests that it is a highly effective drug for the treatment of coronary-artery spasm and variant angina.
Afterload reduction in chronic asymptomatic aortic regurgitation might retard left ventricular enlargement and hypertrophy and, consequently, delay the onset of myocardial dysfunction and the need for surgical intervention. Since afterload is best expressed as wall stress, the effect of nitroglycerin on wall stress was determined in 10 normal subjects and in eight asymptomatic subjects with aortic regurgitation and normal left ventricular and circulatory function. Peak and end-systolic wall stress were estimated using a noninvasive echocardiographic technique. At rest, despite significantly larger left ventricular dimensions in the subjects with aortic regurgitation, peak systolic wall stress in this group (134 +/- 29 X 10(3) dynes/cm2) was similar to that in normal subjects (134 +/- 26 X 10(3) dynes/cm2). In contrast, end-systolic wall stress was higher in aortic regurgitation (84 +/- 12 versus 59 +/- 15 X 10(3) dynes/cm2) (P less than 0.01). Following the administration of nitroglycerin, the subjects with aortic regurgitation had larger reductions in left ventricular end-diastolic (3.5 mm) and end-systolic (3.1 mm) dimensions than did the normal subjects (0.6 and 1.1 mm, respectively), despite similar changes in blood pressure. This resulted in normalization of end-systolic wall stress and in reduction of peak systolic wall stress below normal in aortic regurgitation. We conclude that (1) nitroglycerin offers a simple and effective means of acutely reducing afterload in asymptomatic aortic regurgitation; (2) left ventricular dimensional changes after the administration of nitroglycerin are larger in subjects with aortic regurgitation than in normal subjects. Consequently, unloading therapy may be effective in protecting the left ventricle in this disorder.
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