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Biomedical subjects

W Grossman

Publications and source records attributed to W Grossman.

At least 91 records · Page 5Linked to original sources
PubMed1988

Time course of left ventricular dilation after myocardial infarction: influence of infarct-related artery and success of coronary thrombolysis.

Dilation of the left ventricle after myocardial infarction is common, occurs rapidly (within 2 weeks of infarction) and may be self-limited. To evaluate the time course of postinfarction left ventricular dilation and to assess the impact of successful coronary thrombolysis, serial radionuclide left ventricular volume analyses were performed in 36 patients undergoing attempted thrombolysis for acute transmural myocardial infarction. All patients underwent cardiac catheterization, coronary angiography and attempted thrombolysis within 7 h of the onset of symptoms. The site of coronary occlusion was the left anterior descending coronary artery in 17 patients, the right coronary artery in 18 and, in 1 patient, occluded bypass grafts to the right and left circumflex coronary arteries. Attempted reperfusion using a thrombolytic agent was successful in 22 individuals, occurring 5 +/- 1 h after the onset of symptoms. Gated radionuclide ventriculography was performed early (mean time 1 day after admission, n = 36), subacutely (mean time 11 days postinfarction, n = 36) and late after infarction (mean time 10.5 months, n = 25), and a geometric technique was used to measure serial left ventricular end-diastolic volume. Left ventricular end-diastolic volume for the entire group increased significantly (p less than 0.01) from 153 +/- 30 ml at baseline to 172 +/- 45 ml (at 11 days) to 220 +/- 63 ml (at 10.5 months). Twenty of 36 patients showed greater than 20% increase in left ventricular end-diastolic volume (dilation) with time. This appeared early in seven patients, occurred remote from infarction in seven others and showed a progressive pattern in six.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Combined aortic and mitral balloon valvuloplasty in patients with critical aortic and mitral valve stenosis: results in six cases.

Six patients with severe combined aortic and mitral valve stenosis underwent double valve balloon dilation as an alternative to surgical valve replacement. Cardiac catheterization in all patients before valve dilation revealed heavily calcified aortic and mitral valves with severe stenosis and minimal regurgitation. Balloon aortic valvuloplasty was performed in each patient with a 20 mm balloon dilation catheter passed retrograde through the aortic valve whereas mitral valvuloplasty was performed transseptally with either a single or double balloon technique. After dilation, the mean aortic and mitral gradients decreased in all patients, with the area of the aortic and the mitral valve increasing from 0.5 +/- 0.3 to 0.9 +/- 0.3 cm2 and from 0.7 +/- 0.1 to 1.5 +/- 0.7 cm2, respectively. The procedures were well tolerated, with no embolic events and no significant increase in valvular regurgitation, and resulted in a reduction in symptoms of dyspnea on exertion and weakness in all patients that has persisted for an average of 5.7 months of follow-up in five of the six patients. It is concluded that combined dilation of stenotic aortic and mitral valves can be accomplished percutaneously and may be considered for patients with combined valvular stenosis who refuse or are deferred from surgical intervention.

Aged↗
PubMed1988

Improvement in symptoms and left ventricular performance after balloon aortic valvuloplasty in patients with aortic stenosis and depressed left ventricular ejection fraction.

The application of balloon aortic valvuloplasty to elderly patients with severe aortic stenosis and a low ventricular ejection fraction is undefined. Balloon aortic valvuloplasty was performed in a subset of 28 patients with low left ventricular ejection fraction (37 +/- 11%), severe aortic stenosis, and a mean age of 79 +/- 5 years. After valvuloplasty, significant increases were seen in aortic valve area (from 0.5 +/- 0.1 to 0.9 +/- 0.2 cm2), aortic systolic pressure (from 120 +/- 12 to 135 +/- 22 mm Hg), and cardiac output (from 4.2 +/- 1.1 to 4.8 +/- 1.6 l/min) (p less than 0.01), and significant decreases were seen in transaortic pressure gradient (from 69 +/- 25 to 35 +/- 15 mm Hg) and pulmonary capillary wedge pressure (from 24 +/- 9 to 20 +/- 7 mm Hg) (p less than 0.01). All patients had symptomatically improved at the time of discharge. Serial radionuclide ventriculography showed an increase in left ventricular ejection fraction from 37 +/- 11% before valvuloplasty to 44 +/- 14% within 48 hours after dilatation and to 49 +/- 13% at 3 months after dilatation. However, there was substantial heterogeneity of response. Thirteen patients (group A) showed progressive increases in left ventricular ejection fraction (from 34 +/- 11% to 49 +/- 15% to 58 +/- 11%, p less than 0.0001), whereas 15 patients (group B) showed no significant change in ejection fraction (from 41 +/- 10% to 40 +/- 13% to 41 +/- 10%, p = NS) over 3 months. There was no difference between these groups with respect to age, extent of coronary artery disease, history of myocardial infarction, and aortic valve area before and after valvuloplasty. However, peak systolic wall stress and left ventricular dimensions were higher in group B compared with group A. In conclusion, balloon aortic valvuloplasty may result in symptomatic improvement in patients with aortic stenosis and depressed left ventricular ejection fraction; some patients develop progressive increases in ejection fraction, whereas others fail to show improvement.

Aged↗
PubMed1988

Effect of age on myocardial adaptation to volume overload in the rat.

To test the hypothesis that the capacity for left ventricular (LV) adaptation to volume overload might diminish with age, we examined the hemodynamics and degree of myocardial hypertrophy in response to aortic insufficiency in young adult (9 mo) and old (18 or 22 mo) Fischer rats. Before, immediately after, and at 2 and 4 wk after creating aortic insufficiency, LV and aortic pressures were measured using a catheterization technique. 4 wk after surgery, we measured aortic flow, and estimated the LV passive pressure-volume relationship and the degree of LV hypertrophy after killing. Immediately after the surgical creation of aortic insufficiency, both young and old rats showed similar elevation of LV end-diastolic pressure (from 4.8 +/- 0.6 to 12.0 +/- 1.5 mmHg in the young rats, P less than 0.01; from 4.9 +/- 0.4 to 11.0 +/- 0.7 mmHg in the old rats, P less than 0.01). In the young rats LV, end-diastolic pressure decreased to 8.0 +/- 1.0 and to 8.5 +/- 0.9 mmHg at 2 and 4 wk (P less than 0.05). In contrast, LV end-diastolic pressure at 2 (16.9 +/- 3.1 mmHg) and 4 wk (16.1 +/- 2.7 mmHg) in the old rats was even higher, compared with the values measured immediately after aortic insufficiency. At 4 wk, LV end-diastolic meridional wall stress (calculated from the in vivo LV end-diastolic pressure, and the pressure-volume relationship and muscle mass obtained after killing) was higher in the old rats than in the young rats. In the young rats, the diastolic pressure-volume relationship at 4 wk shifted to the right (P less than 0.01), and LV dry weight, LV dry weight/tibial length, and protein content of the LV myocardium increased by 26% (P less than 0.01), 24% (P less than 0.01), and 33% (P less than 0.01), respectively. However, old rats with aortic insufficiency did not show a significant change in the pressure-volume relationship, dry weight, or protein content at 4 wk. These results suggest that advanced age diminishes the capacity for LV hypertrophy in response to a volume overload, and this reduced LV hypertrophic response in the old rats resulted in persistent elevation of LV end-diastolic pressure and wall stress.

Adaptation, Physiological↗
PubMed1988

Depression of systolic and diastolic myocardial reserve during atrial pacing tachycardia in patients with dilated cardiomyopathy.

Previous reports have shown that increases in heart rate may result in enhanced left ventricular (LV) systolic and diastolic performance. To assess whether this phenomenon occurs in the presence of depressed LV function, the effects of pacing on LV pressure and volume were compared in seven patients with dilated cardiomyopathy (LV ejection fraction 0.19 +/- 0.11) and six patients with no or minimal coronary artery disease (LV ejection fraction 0.69 +/- 0.11). Patients with normal LV function demonstrated significant increases in LV peak-positive dP/dt, LV end-systolic pressure-volume ratio, LV peak filling rate, and a progressive leftward and downward shift of their pressure-volume diagrams, compatible with increased contractility and distensibility in response to pacing tachycardia. There was no change in LV peak-negative dP/dt or tau. Patients with dilated cardiomyopathy, in contrast, demonstrated no increase in either LV peak-positive dP/dt or the end-systolic pressure-volume ratio, and absence of a progressive leftward shift of their pressure-volume diagrams. Moreover, cardiomyopathy patients demonstrated no increase in LV peak-negative dP/dt or LV peak filling rate and a blunted downward shift of the diastolic limb of their pressure-volume diagrams. Tau, as determined from a derivative method, became abbreviated although never reaching control values. We conclude that patients with dilated cardiomyopathy may demonstrate little or no significant enhancement in systolic and diastolic function during atrial pacing tachycardia, suggesting a depression of both inotropic and lusitropic reserve.

Cardiac Output↗
PubMed1987

Diastolic relaxation abnormalities during ischaemia and their association with high energy phosphate depletion, intracellular pH and myocardial blood flow.

Diastolic relaxation of cardiac muscle is an energy requiring process dependent upon restoration of a very low cytosolic calcium concentration. During demand ischaemia, induced by an increase in myocardial oxygen demand in the setting of restricted coronary blood flow, myocardial relaxation is impaired with a resultant decrease in left ventricular chamber distensibility. Metabolic studies suggest that high energy phosphate depletion alone cannot account for these relaxation abnormalities. Changes in myocardial pH and coronary blood flow modulate the impaired relaxation. The most likely hypothesis to explain impaired relaxation during demand ischaemia is that slow calcium uptake and incomplete calcium sequestration are characteristic of the physiology of angina pectoris and demand ischaemia, underlying the increased diastolic stiffness seen in these conditions.

Angina Pectoris↗
PubMed1987

A method for recording isometric tension development by isolated cardiac myocytes: transducer attachment with fibrin glue.

The purpose of this study was to develop a method for attachment of single isolated cardiac myocytes to a transducer for recording isometric tension development. Cardiac myocytes were isolated from the hearts of the toad, Bufo marinus or ferrets by enzymatic digestion with collagenase. The method that we used provided a 60-80% yield of Ca++-tolerant cells. A suspension of cells was placed into a superfusion chamber coated with bovine thrombin. Two glass microtools - each attached to a micromanipulator - were brought into proximity with the ends of a single myocyte; one of the microtools was attached to the element of a low-level force transducer. Human fibrinogen was loaded into a fine-tipped glass micropipette mounted on a micromanipulator. Small amounts of fibrinogen were pressure-ejected from the pipette at each junction between the microtool and the end of the myocyte. The fibrin that formed produced a stable attachment of the ends of the myocyte to the microtools. The myocyte could subsequently be stretched and a length-tension curve recorded. We have used this method to record concentration-dependent tension development in response to the Ca++-ionophore, A23187, and potassium depolarization. Our results indicate that fibrin glue may facilitate the study of the mechanical properties of isolated myocytes.

Animals↗
PubMed1987

Dynamic left ventricular outflow tract obstruction when the anterior leaflet is retained at prosthetic mitral valve replacement.

Dynamic left ventricular outflow tract obstruction developed in a patient in whom the anterior leaflet was retained at mitral valve replacement. It was caused by systolic anterior movement of the native anterior leaflet. Reduced outflow tract diameter, resulting from both posterior displacement of the septum and anterior displacement of the native anterior leaflet by porcine stents, was likely instrumental in promoting dynamic obstruction.

Adult↗
PubMed1987

Postmortem and intraoperative balloon valvuloplasty of calcific aortic stenosis in elderly patients: mechanisms of successful dilation.

Percutaneous balloon dilation of the aortic valve has recently been proposed as a palliative procedure for treating nonsurgical candidates with calcific aortic stenosis. To assess the safety, efficacy and mechanisms of successful balloon valvuloplasty, postmortem (n = 33) and intraoperative (n = 6) balloon aortic valvuloplasty was performed in the hearts of 39 elderly patients with calcific aortic stenosis. The cause of aortic stenosis was degenerative nodular calcification in 28 cases, calcific bicuspid aortic stenosis in 8 cases and rheumatic heart disease in 3 cases. Balloon dilation was performed with 15 to 25 mm balloons in the postmortem specimens, and with 18 to 20 mm balloons in the operating room immediately before aortic valve replacement. After balloon dilation, valve orifice dimensions and leaflet mobility increased in all patients. The mechanisms of successful dilation included fracture of calcified nodules in 16 aortic valves, separation of fused commissures in 5 valves, both in 6 valves and grossly inapparent microfractures in 12 valves. Valve leaflet avulsion occurred in one heart after inflation with a clearly oversized balloon. Liberation of calcific debris, valve ring disruption or midleaflet tears did not occur in any heart. In conclusion, there are at least three mechanisms of successful aortic valvuloplasty, depending on the origin of valvular stenosis. Embolic phenomena and acute valvular regurgitation do not appear to be likely events associated with this procedure.

Aged↗
PubMed1987

Deficient production of cyclic AMP: pharmacologic evidence of an important cause of contractile dysfunction in patients with end-stage heart failure.

We studied the effects of different classes of inotropic drugs on human working myocardium in vitro that was isolated from the hearts of patients with end-stage heart failure, and compared the responses to these drugs with those noted in muscles from nonfailing control hearts. Although peak isometric force generated in response to increased extracellular calcium reached control levels in the muscles from patients with heart failure, the time course of contraction and rate of relaxation were greatly prolonged. The inotropic effectiveness of the beta-adrenergic agonist isoproterenol and the phosphodiesterase inhibitors milrinone, caffeine, and isobutylmethylxanthine was markedly reduced in muscles from the patients with heart failure. In contrast, the effectiveness of inotropic stimulation with acetylstrophanthidin and the adenylate cyclase activator forskolin was preserved. After a minimally effective dose of forskolin was given to elevate intracellular cyclic AMP levels, the inotropic responses of muscles from the failing hearts to phosphodiesterase inhibitors were markedly potentiated. These data indicate that an abnormality in cyclic AMP production may be a fundamental defect present in patients with end-stage heart failure that can markedly diminish the effectiveness of agents that depend on generation of this nucleotide for production of a positive inotropic effect.

1-Methyl-3-isobutylxanthine↗
PubMed1987

Combined percutaneous aortic valvuloplasty and transluminal coronary angioplasty in adult patients with calcific aortic stenosis and coronary artery disease.

Of 120 consecutive balloon aortic valvuloplasty procedures for critical aortic stenosis, valvuloplasty was performed in combination with coronary angioplasty in nine patients (average age 76 years). All nine patients were symptomatic with angina and congestive heart failure before combined procedures. Aortic valvuloplasty was performed with 20 to 23 mm balloon catheter advanced retrogradely from the femoral artery and resulted in an improvement in peak aortic valve gradient (60 +/- 19 to 33 +/- 13 mm Hg; p less than or equal to .01) and calculated aortic valve area (0.7 +/- 0.1 to 1.1 +/- 0.3 cm2; p less than or equal to .01). Single-vessel coronary angioplasty was performed via the femoral approach, with 2.0 to 3.5 mm balloon catheters, and resulted in a mean reduction of a critical coronary stenosis in each patient from 91 +/- 4% to 29 +/- 8%. The site of coronary angioplasty was the left anterior descending artery in three patients, the circumflex artery in three patients, the right coronary artery in two patients, and a bypass graft to the right coronary artery in one patient. Combined procedures were performed with a mean arterial time of 108 min. Complications included groin hematomas (n = 2), transient left bundle branch block (n = 1), and transient atrial fibrillation (n = 1). No patient experienced prolonged chest pain, myocardial infarction, major increase in aortic insufficiency, or embolic phenomena. Eight of the nine patients treated with combined procedures noted significant improvement in symptoms of angina and congestive heart failure and were discharged.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Abnormal intracellular calcium handling in myocardium from patients with end-stage heart failure.

Intracellular Ca2+ release and reuptake are essential for contraction and relaxation of normal heart muscle. Intracellular Ca2+ transients were recorded with aequorin during isometric contraction of myocardium from patients with end-stage heart failure. In contrast to controls, contractions and Ca2+ transients of muscles from failing hearts were markedly prolonged, and the Ca2+ transients exhibited 2 distinct components. Muscles from failing hearts showed a diminished capacity to restore low resting Ca2+ levels during diastole. These experiments provide the first direct evidence from actively contracting human myocardium that intracellular Ca2+ handling is abnormal and may cause systolic and diastolic dysfunction in heart failure.

Adolescent↗
PubMed1987

Effect of age on the development of cardiac hypertrophy produced by aortic constriction in the rat.

To test the hypothesis that the capacity to develop left ventricular (LV) hypertrophy might diminish with advancing age, we examined the hypertrophic response to ascending aortic constriction in 3 groups of adult Fischer 344 rats (9 months, 18 months, and 22 months of age). Aortic constriction was created so that aortic cross-sectional areas would be the same for the 3 groups of rats. Four weeks after imposition of aortic constriction, there was no significant difference in peak LV pressure, peak-to-peak and mean systolic pressure gradients between left ventricle and aorta, cardiac output, LV minute work, or cross-sectional area of the aortic constrictions in the 3 groups. In 9-month-old aortic-constricted rats, LV dry wt (LVDW)/body wt, LVDW/tibial length, and myocyte width increased by 23% (p less than 0.01), 14% (p less than 0.01), and 27% (p less than 0.01), respectively, compared with sham-operated rats. In contrast, in 18-month-old and 22-month-old aortic-constricted rats, LVDW/body wt and LVDW/tibial length were unchanged compared with sham-operated controls, and increases in myocyte width were only modest 4 weeks following constriction. RNA concentration in the myocardium 5 days after constriction increased by 21% (p less than 0.001) in 9-month-old rats but showed no significant rise in 18-month-old rats. These results suggest that advancing age is associated with a diminished capacity to develop myocardial hypertrophy in response to acute pressure overload and that a reduced ability to synthesize protein may be one of the major contributing factors to a diminished capacity for hypertrophy in advanced age.

Aging↗
PubMed1986

Percutaneous mitral valvuloplasty in an adult patient with calcific rheumatic mitral stenosis.

A 75 year old man with long-standing rheumatic mitral stenosis who refused surgical intervention was treated with percutaneous balloon valvuloplasty. Prevalvuloplasty evaluation revealed a heavily calcified mitral valve, a mean transvalvular gradient of 18 mm Hg, a Fick cardiac index of 1.7 liters/min per m2, a mitral valve area of 0.6 cm2 and 1 + mitral regurgitation. After transeptal catheterization and balloon dilation of the interatrial septum with an 8 mm angioplasty balloon, a 25 mm valvuloplasty balloon was advanced over a guide wire across the interatrial septum and positioned across the mitral anulus. Subsequent balloon inflation at 3 atm pressure resulted in a reduction of the mean mitral valve gradient to 12 mm Hg, an increase in cardiac index to 2.5 liters/min per m2, an increase in mitral valve area in 1.4 cm2 and an increase in mitral regurgitation from 1 + to 2 +. Valvuloplasty was well tolerated without embolization of clot or valvular debris, and resulted in marked clinical improvement with decreased dyspnea and increased exercise tolerance. Repeat catheterization 2 months after valvuloplasty showed further resolution of pulmonary hypertension and no evidence of valvular restenosis or worsening mitral regurgitation, but detected a small atrial septal defect with a pulmonary to systemic blood flow ratio of 1.8. It is concluded that percutaneous valvuloplasty is possible in the adult patient with calcific rheumatic mitral stenosis, and may result in a significant improvement in valvular function without producing life-threatening complications.

Aged↗
PubMed1986

Assessment of left ventricular end-systolic pressure-volume relations with an impedance catheter and transient inferior vena cava occlusion: use of this system in the evaluation of the cardiotonic effects of dobutamine, milrinone, Posicor and epinephrine.

The end-systolic pressure-volume relation has been postulated as a load-independent measure of cardiac contractility, but has been difficult to measure because of technical problems associated with the serial measurement of intracardiac volume over a physiologic range of ventricular loading conditions. Utilizing a multielectrode impedance catheter to assess continuous, on-line left ventricular relative volume during transient inferior vena cava occlusion, a method is described for determining the end-systolic pressure-volume relation and for assessing changes in this relation secondary to inotropic modulation. In particular, using this method, the relative inotropic properties were determined of four drugs: dobutamine, milrinone, epinephrine and an experimental cardiotonic agent (Ro 13-6438, Posicor). Left ventricular micromanometer pressure and impedance catheter volume were measured continuously in 10 open chest, anesthetized dogs and 14 pigs. Arterial pressure was altered over a range of 20 to 60 mm Hg by brief inferior vena cava constriction. A linear end-systolic pressure-volume relation was observed in pressure-volume diagrams constructed from on-line pressure and impedance catheter recordings. Administration of dobutamine, milrinone and epinephrine resulted in a leftward shift and an increase in the slope of the end-systolic pressure-volume relation as compared with baseline; Posicor did not alter the slope over a range of doses, despite an increase in the cardiac output secondary to arterial vasodilation. Volume changes as measured by the impedance method closely paralleled simultaneous changes in the ultrasonic crystal-determined segment length, and the impedance end-systolic pressure-volume relation slope was reproducible with repeated load-altering maneuvers.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Survival of patients with severe congestive heart failure treated with oral milrinone.

The safety and efficacy of long-term oral milrinone therapy were evaluated over a 2 1/2 year period in 100 patients who had severe congestive heart failure despite conventional therapy. Long-term oral milrinone therapy (27 +/- 8 mg/day initial dose) was well tolerated; drug-related side effects occurred in only 11% of patients and led to drug withdrawal in only 4% of patients. Of 94 patients evaluated after 1 month of therapy, 51% had improved by at least one New York Heart Association functional class. Despite hemodynamic and clinical improvements, life table analysis showed a 39% mortality rate at 6 months and a 63% mortality rate at 1 year of therapy. Characteristics at study entry that predicted death within 6 months included more advanced functional class, impaired renal function, lower right ventricular ejection fraction, presence of nonsustained ventricular tachycardia on 24 hour ambulatory electrocardiography, more impaired baseline hemodynamic function and absence of clinical improvement after 1 month of milrinone therapy. Multivariate analysis selected lower baseline cardiac index and aortic systolic pressure as the most significant variables in predicting death; patients who died of progressive heart failure had less frequent use of antiarrhythmic drugs and greater increases in furosemide and milrinone doses during long-term follow-up than did those who died suddenly. Thus, although milrinone is well tolerated and produces early symptomatic benefits in approximately half of patients with congestive heart failure refractory to conventional therapy, there is no evidence that it improves the high baseline mortality in this disorder.

Administration, Oral↗