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Biomedical subjects

J L Weiss

Publications and source records attributed to J L Weiss.

At least 73 records · Page 4Linked to original sources
PubMed1988

Immediate enhancement of left ventricular relaxation by coronary artery bypass grafting: intraoperative assessment.

We investigated the effect of coronary artery bypass grafting on the rate of left ventricular relaxation as defined by the time constant for isovolumetric relaxation, T, measured in milliseconds. Completeness of relaxation at rapid heart rates was determined by comparison of the relationship between left ventricular pressure and echocardiographic left ventricular cross-sectional cavity area during rapid ventricular pacing with that obtained after a prolonged diastole when the ventricle was maximally relaxed. Twelve patients with coronary artery disease had significantly higher T values (94.5 +/- 6.2) than six patients without coronary artery disease who were undergoing other open heart procedures (39.5 +/- 5.0, p less than .001). T was significantly reduced after coronary artery bypass grafting (68.2 +/- 5.1, p = .007), but was unchanged in the six control patients after cardiopulmonary bypass (37.8 +/- 4.5, p = .54). Similar changes were found during rapid pacing to 100, 120, and 140/min. Incomplete relaxation was detected in three of 10 (heart rate 120 beats/min) and nine of 11 (heart rate 140 beats/min) patients with coronary artery disease and this decreased to 0 of 10 (heart rate 120 beats/min) and six of 11 (heart rate 140 beats/min) patients after coronary artery bypass. Incomplete relaxation before bypass at a heart rate of 120 beats/min averaged 0.9 +/- 0.3 mm Hg. At a heart rate of 140 beats/min, incomplete relaxation averaged 5.6 +/- 1.6 mm Hg before and 1.4 +/- 0.5 mm Hg after bypass. Intake of beta-blockers or calcium-channel blockers, body temperature, and systolic blood pressure were not found to be related to these changes. We conclude that immediately after coronary artery bypass relaxation of left ventricular muscle is enhanced and incomplete relaxation at rapid heart rates is less likely. The most probable cause of this improvement in ventricular relaxation after coronary artery bypass grafting is relief of ischemia.

Blood Vessel Prosthesis↗
PubMed1988

Cyclic elevation of intrathoracic pressure can close the mitral valve during cardiac arrest in dogs.

Mitral valve closure during cardiopulmonary resuscitation may result from direct cardiac compression. An alternative hypothesis is that with a rise in intrathoracic pressure, mitral valve closure can occur but may be influenced by whether the lungs are inflated or deflated. To test this hypothesis, we placed a large-bore cannula into the thoraces of 11 dogs. Intrathoracic pressure was changed by inflating and deflating the thorax through the cannula while the airway was open, as well as by inflating and deflating the lungs with the thoracic cannula clamped. Mitral valve motion was observed with two-dimensional echocardiography from the right chest wall or esophagus in eight of the dogs. With a rise in intrathoracic pressure from thoracic inflation, all eight dogs showed closure of the mitral valve, while with thoracic deflation, all showed mitral valve opening. With lung inflation and deflation alone, however, the mitral valve remained open throughout the cycle. In seven dogs, with thoracic inflation, the peak gradient from the left ventricle to the left atrium was (mean +/- SEM) 18 +/- 4 mm Hg and the average gradient was 7 +/- 3 mm Hg, while with lung inflation alone, the average gradient was -1 +/- 1 mm Hg (p less than 0.01 vs. thoracic inflation). Thus, mitral valve closure, with concomitant retrograde pressure gradients, can be produced by intrathoracic pressure changes with accompanying lung deflation. With lung inflation alone, however, the mitral valve remains open, and there are no significant transmitral pressure gradients. We conclude that intrathoracic pressure changes can cause the mitral valve to close or to remain open, depending on how intrathoracic pressure is generated.

Animals↗
PubMed1987

A randomized trial of intravenous tissue plasminogen activator for acute myocardial infarction with subsequent randomization to elective coronary angioplasty.

Patients presenting within four hours of the onset of acute myocardial infarction were randomly assigned to receive 80 to 100 mg of recombinant human-tissue plasminogen activator (t-PA) intravenously over a period of three hours (n = 72) or placebo (n = 66). Administration of the study drug was followed by coronary arteriography, and candidates for percutaneous transluminal coronary angioplasty were randomly assigned either to undergo angioplasty on the third hospital day (n = 42) or not to undergo angioplasty during the 10-day study period (n = 43). The patency rates of the infarct-related arteries were 66 percent in the t-PA group and 24 percent in the placebo group. No fatal or intracerebral hemorrhages occurred, and episodes of bleeding requiring transfusion were observed in 7.6 percent of the placebo group and 9.8 percent of the t-PA group. As compared with the use of placebo, administration of t-PA was associated with a higher mean (+/- SEM) ejection fraction on the 10th hospital day (53.2 +/- 2.0 vs. 46.4 +/- 2.0 percent, P less than 0.02), an improved ejection fraction during the study period (+3.6 +/- 1.3 vs. -4.7 +/- 1.3 percentage points, P less than 0.0001), and a reduction in the prevalence of congestive heart failure from 33 to 14 percent (P less than 0.01). Angioplasty improved the response of the ejection fraction to exercise (+8.1 +/- 1.4 vs. +1.2 +/- 2.2 percentage points, P less than 0.02) and reduced the incidence of postinfarction angina from 19 to 5 percent (P less than 0.05), but did not influence the ejection fraction at rest. These data support an approach to the treatment of acute myocardial infarction that includes early intravenous administration of t-PA and deferred cardiac catheterization and coronary angioplasty.

Angina Pectoris↗
PubMed1987

Geometric considerations in determination of left ventricular mass by two-dimensional echocardiography.

This review describes the technique of and advances in determination of left ventricular mass by two-dimensional echocardiography. Two-dimensional echocardiographic model systems, which require geometric assumptions, may have limited accuracy in mass determination if ventricular shape is deformed or the architecture is irregular, as it may be in various disease states. Recently developed techniques allow free angulation of the echocardiographic transducer with continuous recordings of the three-dimensional coordinates of each image without imposing restraints on transducer orientation. These developments have led to methods for accurate three-dimensional reconstruction of left ventricular mass, even in the presence of severe dilatation or deformity. With the interaction of two-dimensional echocardiography, a coordinate system for locating the transducer in three-dimensional space, and computer-aided echocardiographic contouring, it is possible to obtain left ventricular mass estimates with a high degree of accuracy from randomly oriented views without practical restriction on transducer motion or major geometric assumptions.

Cardiac Volume↗
PubMed1986

Absence of left ventricular dysfunction during acute chagasic myocarditis in the rhesus monkey.

Recent studies suggest that intracellular Trypanosoma cruzi invasion with release of intracellular myocardial antigens during T. cruzi infection is crucial to the pathogenesis of chronic chagasic myocarditis. However, in areas endemic for Chagas' disease, the incidence of clinical acute chagasic myocarditis has been reported to be low among infected individuals, while the incidence of chronic chagasic myocarditis is relatively high. Thus, either acute chagasic myocarditis rarely complicates T. cruzi infection and is not important to the pathogenesis of chronic chagasic myocarditis, or acute chagasic myocarditis rarely impairs left ventricular function and therefore causes no symptoms. To investigate this question we innoculated T. cruzi from a human patient with Chagas' disease into the subconjuntivae of six rhesus monkeys (7.5 X 10(3) parasites each). Parasitemia was monitored and weekly two-dimensional echocardiograms (for determination of end-diastolic and fractional change in area, EDA and FCA) were obtained to quantify global left ventricular function for 10 weeks. Regional left ventricular function was assessed by visual analysis of two-dimensional echocardiograms. Extent of acute myocarditis was established at autopsy. All monkeys had the Romaña sign and detectable parasitemia in the second week. Parasitemia rose in all by the ninth week (mean = 1.8 X 10(5) parasites/ml); four monkeys lost weight (mean = -12%), three died, and three were killed. Two-dimensional echocardiographic EDA and FCA remained unchanged from control to the last study within 12 hr of death (EDA = 2.6 +/- 0.9 to 2.7 +/- 1.0 cm2, FCA = 80 +/- 6.8 to 74 +/- 7.6%, NS). Furthermore, regional left ventricular function remained unchanged throughout the period of study.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Septal geometry in the unloaded living human heart.

Right ventricular loading leads to diastolic septal flattening in man without necessarily requiring right ventricular pressure to exceed left ventricular pressure. This observation suggested that the unstressed septal configuration is flat and that its normal concave shape is due to the left-to-right transseptal pressure gradient. To examine this hypothesis, we studied septal configuration by two-dimensional echocardiography in nine patients with normal global and regional left ventricular function during surgery for coronary artery disease. The transseptal pressure gradient was obtained from pulmonary capillary wedge pressure minus right atrial pressure. Measurements were obtained at control (open chest, intact pericardium [C]), with the pericardium open (OP), on cardiopulmonary bypass (CPB), and after cardiac arrest (CA). There were no changes in any measurements between C and OP or between CPB and CA. Left ventricular end-diastolic cavity area decreased from 16.5 +/- 2.1 cm2 at C to 11.1 +/- 4.5 cm2 after CPB, and further decreased to 8.9 +/- 3.5 cm2 after CA (p less than .001), yet the septum flattened, as shown by an increase in its radius of curvature from 1.7 +/- 0.5 cm during C to 2.5 +/- 0.7 cm after CPB, and to 2.9 +/- 1.0 cm after CA (p less than .001), or from 0.4 +/- 0.1 to 0.8 +/- 0.4 to 1.1 +/- 0.5 U (p less than .001) when normalized for cavity area. Diastolic transseptal pressure gradient was reduced from 4.1 +/- 2.3 mm Hg during C to 1.1 +/- 1.8 mm Hg after CPB, and to 0.5 +/- 1.4 mm Hg after CA (p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1986

Reversible cold-induced abnormalities in myocardial perfusion and function in systemic sclerosis.

The effects of peripheral cold exposure on myocardial perfusion and function were studied in 13 patients with scleroderma without clinically evident myocardial disease. Ten patients had at least one transient, cold-induced, myocardial perfusion defect visualized by thallium-201 scintigraphy, and 12 had reversible, cold-induced, segmental left ventricular hypokinesis by two-dimensional echocardiography. The 10 patients with transient perfusion defects all had anatomically corresponding ventricular wall motion abnormalities. No one in either of two control groups (9 normal volunteers and 7 patients with chest pain and normal coronary arteriograms) had cold-induced abnormalities. This study is the first to show the simultaneous occurrence of cold-induced abnormalities in myocardial perfusion and function in patients with scleroderma. The results suggest that cold exposure in such patients may elicit transient reflex coronary vasoconstriction resulting in reversible myocardial ischemia and dysfunction. Chronic recurrent episodes of coronary spasm may lead to focal myocardial fibrosis.

Adult↗
PubMed1985

Value of intraoperative left ventricular microbubbles detected by transesophageal two-dimensional echocardiography in predicting neurologic outcome after cardiac operations.

To determine whether the presence or absence of left ventricular (LV) intracavitary microbubbles during cardiac surgery predicts neurologic sequelae, 82 patients undergoing cardiac surgery were studied using transesophageal 2-dimensional (2-D) echocardiography. Cross-sectional images were recorded just before and immediately after cardiopulmonary bypass and stop frames were reviewed for the presence of microbubbles, rated as: 0 = absent, 1 = fewer than 5/frame, 2 = 10 to 25/frame, 3 = too numerous to count. Microbubbles were detected after cardiopulmonary bypass in 34 patients (41%) and found more often in valvular or other intracardiac manipulations than in coronary revascularization, 30 of 40 vs 4 of 42, respectively (p less than 0.001). When grade 2 or 3 microbubbles were identified (22 of 34 patients), mechanical attempts to eradicate them were not successful. Postoperative follow-up in all patients revealed no new focal neurologic deficits. Prolonged encephalopathy (confusional state more than 72 hours) occurred in 4 of 48 patients with no detectable microbubbles and in 3 of 34 patients with microbubbles (difference not significant). Thus, intracavitary left ventricular microbubbles are often detected during cardiac operations, particularly during valve replacement, but are not predictive of postoperative neurologic complications. This is true even if microbubbles are densely concentrated; attempts to eradicate microbubbles are unsuccessful and may be unnecessary.

Cardiac Surgical Procedures↗
PubMed1985

Relation of mitral valve prolapse to left ventricular size in Marfan's syndrome.

Sporadic recent reports suggest that mitral valve prolapse (MVP) disappears with progressive left ventricular (LV) dilatation. To test this hypothesis, we sought to determine if an inverse relation exists between MVP and LV cavity size on M-mode echocardiograms in 83 patients with Marfan's syndrome. LV end-diastolic dimensions and presence or absence of MVP were determined. Forty-six patients had MVP. Of patients with an LV end-diastolic dimension less than or equal to 5 cm, 90% had MVP; only 19% of the 32 patients with abnormally large (greater than 5.8 cm) end-diastolic dimension had MVP. The prevalence of MVP in patients with an LV end-diastolic dimension of 5.1 to 5.8 cm was 69%. Thus, the prevalence of MVP was inversely related to LV cavity size. To determine whether appearance or disappearance of MVP was associated with decrease or increase in LV cavity size, serial echocardiograms from 67 patients (mean follow-up 42 months, range 3 to 99) were examined. These patients were separated into 3 groups based on changes in the LV end-diastolic dimension of greater than 1 cm over time. Group 1 consisted of 9 patients, all of whom had MVP and normal LV cavity size on their initial study. With subsequent increase in LV end-diastolic dimension (mean 1.42 +/- 0.3), MVP disappeared in 6 of the 9. Conversely, group 2 consisted of 4 patients, all of whom had dilated left ventricles on their initial echocardiogram and no evidence of MVP. After aortic valve replacement, the LV cavity size decreased (mean 2.3 +/- 0.7) and MVP appeared on follow-up studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Applicability of percutaneous transluminal coronary angioplasty to patients with recombinant tissue plasminogen activator mediated thrombolysis.

To test the utility and safety of percutaneous transluminal coronary angioplasty (PTCA) after recombinant tissue plasminogen activator (t-PA), we performed the procedure in all suitable candidates with acute myocardial infarction (MI) who had successful t-PA mediated coronary thrombolysis. Twenty consecutive patients with MI received t-PA after coronary angiographic conformation of total occlusion. Successful recanalization with t-PA was achieved in 13 patients, leaving a residual obstruction of 84 +/- 6% in the nine patients for whom PTCA was attempted at a mean of 21.6 h. Success was achieved in seven patients, leading to a residual lesion of 29 +/- 7%. In the two patients for whom PTCA was unsuccessful, total reocclusion occurred prior to the attempt despite therapy with heparin, aspirin, dipyridamole, and nifedipine. All PTCA procedures were uncomplicated. Serial two-dimensional echocardiography at 10 days, compared to admission, demonstrated infarct zone wall motion index improvement in the patients with successful PTCA (group A, 0.83 +/- 0.36 to 1.46 +/- 0.49) as compared to the 13 patients without thrombolysis or successful PTCA (group B, 0.61 +/- 0.26 to 0.66 +/- 0.39), (P less than 0.05). One patient of group A sustained a massive stroke at 2 weeks after hospital discharge. In the remaining six patients, follow-up exercise testing and/or coronary arteriography demonstrated a negative treadmill test and/or patent infarct vessel, respectively. After successful PTCA, no patient had clinical signs of reocclusion, reinfarction, postinfarction angina, or congestive heart failure. At 9.4 +/- 2 months, all six patients are asymptomatic and have returned to work. Thus, sequential PTCA after t-PA can be performed safely and successfully in patients with MI and this approach may be associated with improved regional function and a favorable post-MI course.

Angioplasty, Balloon↗
PubMed1985

Regional wall motion improvement after coronary thrombolysis with recombinant tissue plasminogen activator: importance of coronary angioplasty.

To evaluate functional recovery in 20 consecutive patients with acute myocardial infarction who received recombinant tissue-type plasminogen activator, serial two-dimensional echocardiograms were performed before and immediately after tissue plasminogen activator administration and at 1 and 10 days postinfarction. Tissue plasminogen activator was administered intravenously (17 patients) or by intracoronary infusion (3 patients) after angiographic confirmation of total occlusion. Reperfusion, documented by angiography, occurred in 13 of the 20 patients. The mean time from onset of chest pain to thrombolysis was 5.1 +/- 1.1 hours. Echocardiograms were evaluated for regional function with a visual semiquantitative scoring system by two independent observers who had no knowledge of patient identity, temporal sequence, therapy or effect of therapy. There was no immediate or 24 hour improvement in wall motion. At day 10 compared with pretreatment, 28 of 33 reperfused infarct zone segments versus 6 of 20 nonreperfused infarct segments demonstrated improved wall motion (p = 0.01). This improvement did not relate to time from onset of chest pain to successful thrombolysis. Of reperfused infarct zone segments in the distribution of coronary artery balloon dilation, 19 of 23 segments exhibited improvement versus 7 of 17 (reperfused, no angioplasty) and 6 of 20 (nonreperfused, no angioplasty) segments (p = 0.001). Infarct zone segments reperfused at the time of ongoing chest pain demonstrated functional recovery compared with segments reperfused in the absence of chest pain (18 of 23 versus 10 of 20, respectively; p = 0.05). Thus, in this uncontrolled series, there was echocardiographically detectable improvement in function of reperfused infarct segments 10 days after coronary thrombolysis with recombinant tissue plasminogen activator.

Adult↗
PubMed1985

Results of a randomized prospective trial of intraaortic balloon counterpulsation and intravenous nitroglycerin in patients with acute myocardial infarction.

A randomized prospective clinical trial compared combined treatment with intraaortic balloon pumping and intravenous nitroglycerin for 4 to 5 days with routine clinical management in 20 patients with extensive myocardium at risk for infarction as evidenced by a thallium defect score of 7.0 units or greater. No significant differences in mortality or clinical outcome were observed between the 10 patients receiving the combined treatment and the 10 receiving routine management. In 14 patients two-dimensional echocardiograms obtained 6 to 24 hours after the onset of symptoms and at follow-up 6 to 16 days later (after completion of combined intraaortic balloon pumping plus nitroglycerin therapy) were analyzed to determine whether infarct segment or noninfarct segment lengths were affected by therapy. Among these 14 patients, 5 (3 receiving the combined therapy and 2 receiving routine management) demonstrated an increase in infarct segment length of greater than 1.0 cm. Mean infarct segment length increased 0.30 +/- 0.44 cm in patients receiving the combined therapy and 0.29 +/- 0.36 cm in patients on routine management (p = NS). In contrast, noninfarct segment length increased greater than 1.0 cm (mean increase 1.20 +/- 0.39) in five of seven patients on routine management but in none of 7 patients receiving intraaortic balloon pumping plus nitroglycerin therapy (mean decrease 0.22 +/- 0.20 cm) (p less than 0.05). No significant differences were noted in left ventricular ejection fraction, as measured by gated blood pool scintigraphy, or thallium perfusion defect score in a comparison of day 1 (pretreatment) with day 4 thallium or day 7 to 14 gated blood pool scintigrams. Thus, in patients with extensive myocardium at risk, it is unlikely that a reduction in mortality or a significant improvement in myocardial perfusion or ventricular function can be obtained by early intervention with intraaortic balloon pumping in combination with nitroglycerin. Although this combined therapy failed to prevent infarct segment lengthening (infarct expansion), the combined afterload-lowering effects of intraaortic balloon pumping and nitroglycerin did appear to prevent dilation or remodeling of noninfarcted segments during the first 2 weeks after acute myocardial infarction.

Adult↗
PubMed1985

Spontaneous mitral valve prolapse in a breeding colony of rhesus monkeys.

Mitral valve prolapse was observed in 26 of 92 animals in a harem breeding colony of rhesus monkeys (Macaca mulatta). The affected animals had a systolic murmur best auscultated over the mitral region with the animal in a sitting position. Mid-to-late systolic clicks were also heard. Phonocardiographic examination also demonstrated systolic murmurs and clicks in six of 16 animals. Twenty-three of the animals were studied by M mode and/or two-dimensional echocardiography. The diagnosis was confirmed in 12 animals that had a murmur during the examination. Electrocardiograms revealed T wave abnormalities in five animals and left or right ventricular hypertrophy in five. Four adult animals that died during the course of the study were confirmed at necropsy as having prolapse of the posterior and/or anterior mitral valve leaflets into the atrium. Analysis of the breeding records suggested that mitral valve prolapse was a dominant genetic trait with an approximate birth incidence of 16% to 20% in the colony. The existence of mitral valve prolapse in a nonhuman primate species provides a unique opportunity to study the disease in an experimental animal.

Animals↗
PubMed1985

Impaired thickening of nonischemic myocardium during acute regional ischemia in the dog.

To study the regional function of nonischemic myocardium after the onset of regional ischemia, graded circumflex coronary arterial stenosis was induced in 18 open-chest anesthetized dogs. Two-dimensional echocardiographic views were obtained at each degree of occlusion in a cross-sectional plane marked by two to three metal beads sewn to the left ventricular epicardium. Percent systolic thickening was measured at 16 equally spaced points around the left ventricle and correlated with microsphere-determined regional myocardial blood flow. Baseline thickening averaged 44.9 +/- 6.4%. During transmural ischemia percent systolic thickening decreased to -16.1 +/- 4.0% in the ischemic region and also decreased in adjacent nonischemic regions (to 2.4 +/- 2.4% in segments closest to the ischemic region [adjacent 1] and to 15.5 +/- 3.9 in segments further away [adjacent 2]), but was unchanged in segments directly opposite the ischemic region (remote region). During subendocardial ischemia, percent systolic thickening fell only in the ischemic and adjacent 1 regions (1.4 +/- 5.2% and 24.9 +/- 5.0%, respectively). Dipyridamole, 0.21 to 0.42 mg/min iv, given to seven dogs during transmural ischemia, caused a three- to fivefold increase in flow to the nonischemic and no change in flow to the ischemic region; function was not altered in any region. Propranolol, 0.1 mg/kg iv, was given to five dogs during transmural ischemia to depress contractility in the remote region. Percent systolic thickening fell in the remote (from 50.0 +/- 7.7% to 34.6 +/- 5.6%), but increased in adjacent 1 (from -0.25 +/- 3.7% to 15.2 +/- 3.9%) and in adjacent 2 (from 17.4 +/- 2.8% to 33.4 +/- 3.9%) regions, and remained unchanged in the ischemic region. We conclude the following: During transmural ischemia percent systolic thickening is markedly impaired in nonischemic myocardium immediately adjacent to the ischemic region, and is impaired to a lesser degree in regions located relatively far from the ischemic border. Dysfunction therefore overestimates the extent of regional ischemia after total coronary occlusion. During subendocardial ischemia function ceases in the ischemic region and functional impairment of nonischemic myocardium is restricted to immediately adjacent regions. Dysfunction of adjacent regions is not caused by "relative ischemia" related to increased local oxygen demands or to a steal phenomenon. Mechanical tethering of nonischemic myocardium adjacent to ischemic regions, secondary to changes in left ventricular shape during contraction, may contribute to the impairment of systolic thickening in adjacent regions during transmural ischemia.

Acute Disease↗