Rosemarie Salerni

Successful reversal by chelation therapy of congestive cardiomyopathy due to iron overload.

A patient who developed severe iron overload cardiomyopathy is described. Venesection could not be performed because the patient had chronic anemia. Deferoxamine mesylate, a chelating agent, was administered daily for more than 2 years and produced significant improvement in ventricular function which was associated with a biopsy-proven decrease in myocardial iron stores. This is the first reported case in which a severe cardiomyopathy due to iron overload was reversed by chelation therapy alone.

Left ventricular hypertrophy in cyclosporine-induced systemic hypertension after cardiac transplantation

Abstract Systemic hypertension usually develops in cyclosporinetreated heart transplant patients. 1 A major independent risk factor for cardiovascular events is left ventricular (LV) hypertrophy, 2 which may be expected with longstanding hypertension. We undertook this study to determine whether LV hypertrophy does develop in this setting, and if so, at what time after transplantation.

Acute hemodynamic effect of oral MDL 17,043 in severe congestive heart failure

MDL 17,043, when administered intravenously in humans, produces a significant and salutary hemodynamic response. To determine its acute effect when administered orally (3 mg/kg), 10 patients with severe congestive heart failure were studied by right-sided cardiac catheterization for 8 hours. At 4 hours after drug ingestion, there was significant improvement in several hemodynamic measurements. Cardiac index increased 38% over baseline (from 1.9 +/- 0.4 to 2.6 +/- 0.4 liters/min/m2, p less than 0.01), arteriovenous oxygen difference decreased by 30% (from 8.0 +/- 1.4 to 5.6 +/- 1.2 vol%, p less than 0.01), heart rate increased by 8% (from 85 +/- 16 to 92 +/- 16 beats/min, p less than 0.05), stroke volume index increased by 22% (from 23 +/- 5 to 28 +/- 4 ml/beat/m2, p less than 0.05), left ventricular stroke work increased by 24% (from 18 +/- 5 to 22 +/- 5 g-m/m2, p less than 0.01), mean arterial pressure decreased by 10% (from 79 +/- 6 to 71 +/- 9 mm Hg, p less than 0.01), mean right atrial pressure decreased by 40% (from 10 +/- 5 to 6 +/- 4 mm Hg, p less than 0.01), and mean pulmonary artery wedge pressure decreased by 36% (from 22 +/- 5 to 14 +/- 6 mm Hg, p less than 0.01). Cardiac index, arteriovenous oxygen difference, mean arterial pressure, right atrial pressure, and pulmonary artery wedge pressure remained significantly improved at 8 hours. These findings indicate that MDL 17,043 is active when administered orally and produces beneficial hemodynamic effects for as long as 8 hours.

Comparison of ambulatory left ventricular ejection fraction and blood pressure in systemic hypertension in patients with and without increased left ventricular mass

To evaluate the effects of long-standing systemic hypertension on left ventricular (LV) function during daily activities, ambulatory radionuclide monitoring of LV ejection fraction (EF) and blood pressure was performed during exercise and other structured activities in 31 hypertensive patients. Patients were divided into 3 groups based on the absence of LV hypertrophy (group 1 [n = 16], LV mass 107 +/- 12 g/m2), presence of LV hypertrophy without electrocardiographic changes (group 2 [n = 10], LV mass 141 +/- 8 g/m2) and LV hypertrophy with associated electrocardiographic changes (group 3 [n = 5], LV mass 158 +/- 9 g/m2). The groups were similar with respect to age, baseline medication, treated and untreated blood pressure, resting EF and treadmill exercise time. Patients in group 3 had the longest history of hypertension. Peak filling rate was normal in group 1 (2.9 +/- 0.4 end-diastolic volume/s), but reduced at rest in groups 2 (2.4 +/- 0.4) and 3 (2.1 +/- 0.3). Patients in group 1 had normal EF responses to exercise and mental stress testing, as well as during routine ambulatory activities. Patients in group 2 had a blunted EF response to exercise, and those in group 3 had a significantly abnormal response. Both group 2 and 3 patients demonstrated abnormal EF responses to mental stress, as well as cold pressor testing in association with significant increases in mean arterial pressure and marked reduction in diastolic filling rate. Decreases in EF were also observed during routine patient monitoring in 3 group 3 patients and 4 group 2 patients. These events were associated with significantly increased blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Delayed Postoperative Cardiac Tamponade: Diagnosis and Management

Symptoms and signs of decreased cardiac output associated with an elevated venous pressure should alert one to the possibility of delayed cardiac tamponade. Enlargement of the cardiothoracic ratio shown by serial roentgenograms and demonstration of significant pericardial effusion by echocardiogram or radionuclide angiocardiography support the diagnosis. Erratic response of the prothrombin time to administration of warfarin and abnormal results of liver function test are additional clues to its diagnosis. Right heart catheterization documents the presence of tamponade and excludes other diagnostic considerations. Operative decompression of the pericardial space can be accomplished by pericardicentesis, subxiphoid pericardiotomy, median sternotomy, or thoracotomy. Hemodynamic observations following the relief of tamponade assure that an adequate therapeutic procedure has been performed.

Electrocardiographically discrete right and left ventricular QRS complexes: A case report

A patient with congestive cardiomyopathy manifested a right ventricular QRS followed after 80 msec. by a left ventricular QRS in response to a single atrial depolarization. The ventricular sequence was reversible when the left ventricle was paced directly. Virtually the entire ipsilateral ventricular ejection period occurred during diastolic filling of the contralateral ventricle. Triggered left ventricular pacing, using the right ventricular electrogram as trigger, shortened the QRSRV-QRSLV interval and resulted in a reduction of left ventricular filling pressure and a significant rise in cardiac output. These findings indicated an independent contribution of this unique form of interventricular conduction disturbance to deterioration in hemodynamic performance.

Noninvasive evaluation of systolic and diastolic function in severe congestive heart failure secondary to coronary artery disease or idiopathic dilated cardiomyopathy

The usefulness of systolic time intervals, diastolic time intervals and echocardiography in evaluating left ventricular (LV) function was determined in 69 patients with severe congestive heart failure. All systolic time intervals were markedly abnormal (preejection period/LV ejection time 0.59 +/- 0.18 vs 0.30 +/- 0.04, preejection period index 170 +/- 37 vs 117 +/- 11, LV ejection time index 372 +/- 26 vs 410 +/- 17; patients vs control subjects, p less than 0.05). Diastolic time intervals in patients were not different from those in control subjects. Echocardiographic measurements were all markedly abnormal (LV end-diastolic dimension 6.9 +/- 1.0 vs 4.8 +/- 0.4 cm, patients vs control subjects, p less than 0.05). No pattern of abnormalities distinguished ischemic cardiomyopathies from idiopathic dilated cardiomyopathies. The presence of LV conduction delay did not substantially alter results, except that exclusion of patients with LV conduction delay normalized the total time of systole (QA2) index (from 542 +/- 40 to 531 +/- 31 ms) and reduced but did not normalize prolongation in the preejection period index (from 170 +/- 37 to 162 +/- 29 ms). No systolic or diastolic interval strongly correlated with any hemodynamic or other independent measure of LV performance. Twenty-four patients were given inotropic or unloading agents, which significantly improved hemodynamic values. Systolic and diastolic intervals were measured at baseline and at maximal hemodynamic effect. The correlation of changes in hemodynamics with changes in systolic and diastolic intervals was only modest. Thus, although systolic time intervals and associated echocardiographic measurements can detect abnormal LV function, they cannot reliably detect a change in LV function or distinguish gradations of abnormality.(ABSTRACT TRUNCATED AT 250 WORDS)

Echophonocardiographic estimates of pulmonary artery wedge pressure in mitral stenosis

The efficacy of noninvasive indexes for predicting pulmonary artery wedge (PAW) pressure was reviewed in 77 patients with mitral stenosis. M-mode echocardiography and phonocardiography were used to measure the aortic valve closure-mitral valve E-point interval (A2-E) and the electrocardiographic Q wave-mitral valve closure interval (Q-C) close to the time of diagnostic cardiac catheterization. During catheterization, in 65 patients PAW pressure was measured and in 12 left atrial (LA) pressure was measured. The A2-E and Q-C intervals taken alone had only modest correlation with PAW pressure (r = -0.54 and r = 0.46, respectively). The correlation was weakest in patients with atrial fibrillation and best in sinus rhythm when heart rate variation between invasive and noninvasive studies was within +/- 5 beats. Substitution of V-wave pressure for mean PAW pressure and correction for variation in blood pressure improved the A2-E correlation (r = -0.64), as did combining the A2-E and Q-C intervals into a ratio [(Q-C)/(A2-E)] (r = 0.62). However, the best results were obtained in patients where LA pressure was measured directly (r = -0.91 for A2-E), suggesting the PAW pressure is not always an accurate reflection of LA pressure. In conclusion, many factors in addition to LA pressure affect the Q-C and A2-E intervals which, in many situations, decrease their predictive value. However, if used appropriately, these intervals may allow an estimation of PAW pressure.

The noninvasive assessment of pulmonary capillary wedge pressure in mitral regurgitation

The interval between the aortic closure sound and the mitral opening snap (A2-OS) has been shown to have a significant inverse correlation with pulmonary capillary wedge pressure (PCW) in mitral stenosis. The present study critically examines the relationship of several noninvasively determined diastolic intervals to PCW in patients with relatively pure mitral regurgitation (MR). Fifty-seven patients with MR of diverse etiologies were studied with echocardiograms and phonocardiograms in addition to right and left heart catheterization. Noninvasive determination of the time intervals of aortic closure sound to mitral valve opening (A2-MO), mitral D point to E point (D-E), aortic closure sound to mitral E point (A2-E), the interval from the onset of the QRS to mitral closure (Q-C), and the ratio Q-C/A2-E were compared to invasive measurements of mean PCW, the height of the V wave of PCW (PCW-V), and the ratio of PCW-V to left ventricular (LV) peak systolic pressure (PCW-V/LV). Correlation between each of the five noninvasive intervals and each of the three invasive pressure measurements was then determined. Of the noninvasive intervals studied, A2-MO had the best inverse correlation with all measures of PCW. All 18 patients having a short A2-MO (less than 40 msec) had a PCW-V of greater than or equal to 40 mm Hg and all seven patients having a long A2-MO (greater than 85 msec) had a PCW-V of less than 22 mm Hg. A2-E also had a strong inverse correlation with PCW.(ABSTRACT TRUNCATED AT 250 WORDS)

Pressure and sound correlates of the mitral valve echocardiogram in mitral stenosis

SUMMARY The pressure and sound correlates of the mitral valve echocardiogram (MVE) were investigated in 10 patients with mild to moderate mitral stenosis using high fidelity catheter tip micromanometers. Slow and rapid phases of the MVE anterior motion at the time of opening are associated with the slow and rapid phases of the left atrial y descent. The slow MVE motion and the slow y descent begin during isovolumic left ventricular relaxation when left ventricular pressure still exceeds left atrial pressure. The rapid MVE anterior motion and the rapid y descent begin with pressure crossover. Posterior motion of the MVE at the time of closure also occurs in two phases. After the onset of left ventricular pressure rise at end-diastole, a slow posterior motion is associated with a rising left atrial c wave. Rapid posterior motion begins with pressure crossover and is completed near the peak of the c wave. The fall in left atrial pressure during valve opening can be related to movement of the mitral valve away from the left atrium with the fall in left ventricular (LV) pressure. During valve closure, the rising left atrial (LA) pressure can be related to the ascent of the mitral valve toward the left atrium. Both the mitral component of the first heart sound and the opening snap occur at points of maximum MVE excursion and after LVLA pressure crossover.