Biomedical subjects
Publications and source records attributed to J Meller.
Intrauterine congestive heart-failure caused by a supraventricular tachyarrhythmia was diagnosed in a fetus at 29-30 weeks' gestation. Major congenital malformations were excluded by sonography, amniocentesis, and fetal abdominal paracentesis, and those of the heart by intrauterine fetal echocardiography. The mother was given digoxin and the fetal tachycardia converted to sinus rhythm.
To examine the importance of left ventricular chamber size in determing the response to vasodilator therapy, we performed echocardiography in 40 patients with chronic refractory heart failure before they were treated with oral hydralazine. The left ventricular end-diastolic dimension (LVEDD) correlated significantly with the per cent change in stroke volume (r = 0.77), left ventricular filling pressure (r = -0.68), and stroke work index (r = 0.87) during short-term drug administration. After 14 to 21 days of maintenance therapy, 15 of 24 patients with an LVEDD greater than or equal to 60 mm were improved, and one was worse; mean blood urea nitrogen decreased from 45.6 to 30.6 mg per deciliter in the 21 patients in this group who completed the study (16.3 to 10.9 mmol per liter) (P less than 0.001). In contrast, only two of 16 patients with an LVEDD less than 60 mm improved, whereas 10 showed clinical deterioration; blood urea nitrogen increased from 49.3 to 64.2 mg per deciliter in the 13 patients in this group who completed the study (17.6 to 22.9 mmol per liter) (P less than 0.01). These findings indicate that left ventricular chamber size is an important factor in the response to hydralazine in patients with severe chronic heart failure.
Motion of the posterior aortic root on echocardiography is related to left atrial volume changes. Early diastolic posterior motion of the aortic root reflects both LA emptying and filling and has been measured as the atrial emptying index. To study late diastolic motion of the aortic root, we measured the slope of posterior motion of the aortic root after left atrial systole (following the P wave of the ECG) in 25 subjects without heart disease (Group 1), in 15 patients with left ventricular hypertrophy due to pressure overload (Group 3) with mitral stenosis. The aortic root slope measured (mean +/- SEM) 58.0 +/- 1.9 mm./sec. in Group 1, 50.6 +/- 4.5 mm./sec. in Group 2 (NS vs 1) and 28.8 +/- 4.5 mm./sec. in Group 3, (p < 0.01 vs 1 or 2). In 16 patients (four in Group 1 and 12 in Group 2) studied at catheterization, an inverse correlation ( r = -0.74, p < 0.01) was found between the aortic root slope (over a range of 30 to 73 mm./sec.) and left ventricular late diastolic chamber stiffness measured with simultaneous left ventricular echo and high-fidelity pressure recordings. No correlation was found between this slope and either left atrial size, total aortic root excursion, left ventricular pressure pre "A" wave, height of the A wave, end-diastolic pressure, or the atrial contribution to left ventricular filling. Therefore, the aortic root slope in late diastole is decreased in mitral stenosis and in the absence of mitral stenosis, it appears to be related to late diastolic properties of the left ventricle.
This review is directed at the clinically useful highlights of ultrasound and radionuclide testing in adults with coronary and valvular heart disease, intracardiac shunts, and hypertrophic and congestive cardiomyopathies. As a clinical toto, the radionuclide procedures are currently more useful than ultrasound examination in evaluating patients with known or suspected coronary artery disease. This includes both primary diagnosis and the more accurate estimation of left ventricular function in the presence of segmental asynergy. In patients with valvular disease, the radionuclide procedures are only indirectly useful, while the ultrasound examination is more often diagnostic. These two techniques are complimentary to one another in their ability to noninvasively evaluate and monitor both chamber size and ventricular function in virtually all patients. Recent research involving noninvasive ventricular imaging during physiologic and pharmacologic intervention holds promise for a more sophisticated noninvasive approach to patient management.
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Forty-nine patients undergoing cardiac catheterization for suspected coronary artery disease (CAD) were monitored with a two-channel ambulatory ECG and were given maximal treadmill exercise tests when these were not contraindicated. The ambulatory ECG recordings were evaluated for the number of ST segment deviations after correction for positional changes, and the results were then compared with those of the exercise test and coronary angiography. Sensitivity and specificity of ambulatory ECG monitoring for ST segment deviations to detect CAD were 76% and 75% respectively while those of exercise testing were 78% and 63% respectively. Sixteen patients (33% of this series) had equivocal or contraindicated exercise tests and twelve of these patients were correctly classified as to the presence or absence of CAD by ambulatory ECG. ST segment deviations on ambulatory ECG were found in 93% of patients with three vessel, two vessel, or one vessel LAD disease, while exercise testing detected 74% of these patients. Ambulatory ECG is an effective non-invasive method to diagnose CAD and is complementary to excercise testing. It is of special value when the exercise test is equivocal or contraindicated.
Hemodynamic responses to different doses of hydralazine were evaluated in 18 patients with severe refractory resistant heart failure. There were no significant overall hemodynamic effects after 50 mg hydralazine. After 75 mg, CI increased slightly (+0.36 l/min/m2) with a 19% decrease in SVR. After 100 mg, there were substantial increases in CI (+0.60 l/min/m2) and decreases in SVR (31%) changes which were greater than those after 75 mg, but the decrease in MAP with 100 mg (-6.6 mm Hg) was of the same order as that after 75 mg (-5.0 mm Hg). LVFP and SWI improved significantly only with 100-mg doses. Seven patients in whom 100 mg hydralazine induced no hemodynamic effects all responded to single doses of 150 to 200 mg. The duration of action of hydralazine was longer (p less than 0.001) in patients with a CCr less than 35 ml/min (14.3 +/- 1.4 hr) than in patients with adequate renal function (7.9 +/- 0.5 hr). Thus, the dose and dosing interval of hydralazine needed to induce hemodynamic improvement in patients with severe heart failure are variable and require individualization.
Measurement of stroke volume by pulsed Doppler echocardiography has not been validated against a reference method in vivo. We compared Doppler systolic frequency shift integrals with electromagnetic flowmeter stroke volume in seven open-chest dogs. A pulsed Doppler echocardiographic transducer was held on the aortic arch with the sample volume in the ascending aorta. Stroke volume was varied by epinephrine or pentobarbital infusions, fluid administration or inferior vena caval construction. Linear regression analysis of stroke volume vs Doppler systolic frequency shift integrals revealed strong correlations and intercepts close to zero (tau = 0.74-0.096, rho less than 0.001). Minor changes in transducer position did not influence Doppler frequency shift integrals substantially. Therefore, pulsed Doppler echocardiography served as an excellent measurement of stroke volume changes in model. However, serious limitations are presented that may limit its clinical application.
We studied the hemodynamic events that followed abrupt withdrawal of nitroprusside in 20 patients with severe chronic heart failure. With nitroprusside, cardiac index increased from 1.96 to 2.87 liters per minute per square meter of body-surface area, but it decreased to 1.66 (P less than 0.001) after withdrawal of nitroprusside. Left ventricular filling pressure and systemic vascular resistance decreased from 23.9 to 15.3 mm Hg and from 1642 to 921 dyn.sec.cm-5, respectively, with nitroprusside, but increased to 30.4 mm Hg and 2109 dyn.sec.cm-5 (both P less than 0.001) upon its discontinuation. These rebound changes were maximal 10 to 30 minutes after nitroprusside withdrawal and returned to control levels one to three hours later. Although in 17 of 20 patients, these rebound changes caused no or minimal exacerbation of symptoms, pulmonary edema, which resolved in three patients. Activation of reflex vasoconstrictive forces during vasodilator therapy may explain these effects of withdrawal.
To determine the clinical usefulness of echocardiography in patients with anteroseptal myocardial infarction, echocardiograms were performed within 24 hours of admission on 40 patients with acute transmural anteroseptal myocardial infarction. Twenty-one patients had normal septal motion and septal systolic thickening, and 19 patients had abnormalities of one or both of these measurements. Of the 21 patients who had normal septal motion and thickening, only five developed congestive heart failure, none developed bundle branch block, and none died. Of the 19 patients with abnormal septal motion and/or thickening, 17 developed congestive heart failure (p less than .001), seven developed bundle branch block (p less than .001), and six died (p less than .001). Therefore, (1) electrocardiographic evidence of septal infarction does not correlate with abnormalities of the portion of septum seen on echocardiogram, and (2) patients with anteroseptal myocardial infarction and abnormalities of the septum on echocardiogram have more complications and a higher in-hospital mortality rate. These patients may have more extensive myocardial infarction predisposing to pump failure and possibly involving the conduction system.
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To compare the hemodynamic effects of prazosin and nitroprusside in patients with severe congestive heart failure, nine patients with heart failure refractory to conventional therapy received oral prazosin and intravenous nitroprusside administered so as to produce a similar decrease in left ventricular filling pressure in each patient. By this comparison, both drugs produced similar decreases in mean right atrial pressure, mean pulmonary arterial pressure and systemic and pulmonary vascular resistance. However, with nitroprusside, cardiac index increased more (+0.97 versus +0.73 liters/min per m2, P less than 0.01) and mean arterial pressure decreased less (-13.7 versus -18.3 mm Hg, P less than 0.05) than with prazosin. Both drugs produced similar changes in stroke volume index (+11.7 cc/beat per m2 with nitroprusside and +12.5 with prazosin) and stroke work index (+8.1 g-m/m2 with nitroprusside and +6.6 with prazosin). Therefore, the differences in the hemodynamic responses observed with the two agents were due to the significantly greater decrease in heart rate with prazosin (-8 beats/min) than with nitroprusside (-2 beats/min, P less than 0.05). These clinical data support experimental evidence suggesting that there is a significant negative chronotropic action of prazosin independent of its peripheral vascular effects.
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To study the influence of left ventricular (LV) late diastolic filling on the A wave of the LV pressure, simultaneously recorded echocardiographic LV dimensions and high-fidelity LV pressure measurements were taken in 24 patients. Group 1 comprised eight patients without LV hypertrophy (LVH) and LV end-diastolic pressure (LVEDP) less than or equal to 13 mm Hg. Group 2 comprised 16 patients with LVH secondary to aortic stenosis, idiopathic hypertrophic subaortic stenosis, or hypertension and increased LVEDP. Patients in group 2 had significantly thicker left ventricles, decreased mitral E-to-F slopes, and larger A waves in the LV pressure curve. On the basis of end-diastolic chamber stiffness, we divided group 2 into two populations: 12 patients (group 2A) with end-diastolic chamber stiffness similar to that in group 1, and four patients (group 2B) with markedly elevated end-diastolic chamber stiffness. Patients in group 2A had a larger atrial contribution to LV filling than those with markedly abnormal stiffness (group 2B). Therefore, in LVH an increased A wave in the LV pressure may be related to either elevated end-diastolic chamber stiffness or augmented left atrial volume transport.
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A 37 year man with combined subpulmonic and subaortic idiopathic hypertrophic stenosis proved by cardiac catheterization had typical echocardiographic findings of idiopathic hypertropic subaortic stenosis (IHSS) and systolic anterior motion of the anterior leaflet of the tricuspid valve. This motion of the tricuspid valve may relate to the subpulmonic infundibular gradient in the same way that the systolic anterior motion of the anterior mitral leaflet relates to the subaortic left ventricular gradient in patients with IHSS.
Echocardiography was used to evaluate the late diastolic filling period of the left ventricle in 30 normal individuals, 25 patients with left ventricular hypertrophy, normal sinus rhythm, and either a normal or delayed mitral valve closure, and 15 patients with atrial fibrillation. The echocardiographic ventricular A wave (VAW) was defined as the difference between the end-diastolic and an earlier late-diastolic internal left ventricular dimension, and it was felt to primarily reflect the atrial contribution to late diastolic filling of the left ventricle. It disappeared during ventricular pacing and was significantly smaller than normal in patients with atrial fibrillation. The VAW was significantly larger in patients with left ventricular hypertrophy and normal mitral valve closure reflecting the greater contribution by atrial contraction to late diastolic filling in these patients. In patients with left ventricular hypertrophy and delayed mitral valve closure, the VAW was normal reflecting lesser ventricular enlargement with atrial contraction than in the other patients with left ventricular hypertrophy. This suggested a greater impairment to left ventricular filling in these patients. Therefore, the VAW appears to be an indicator of abnormalities of late diastolic filling caused by left ventricular hypertrophy.
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