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Biomedical subjects

J M Isner

Publications and source records attributed to J M Isner.

At least 325 records · Page 18Linked to original sources
PubMed1982

Left ventricular incision midway between the mitral anulus and the stumps of the papillary muscles during mitral valve excision with or without rupture or aneurysmal formation: analysis of 10 necropsy patients.

Certain clinical and morphologic observations are described in 10 patients who had mitral valve replacement (MVR) and lacerations of the left ventricular (LV) free wall midway between the anulus of the mitral valve and the stumps of the LV papillary muscles. In five patients the lacerations led to LV free wall rupture, with immediate hemopericardium in two and delayed (2 to 4 days) rupture in the other three. Of the other five patients, three developed aneurysm of the LV free wall, the mouth of which was located midway between mitral anulus and papillary muscle stumps, the sites of the lacerations observed in the other seven patients. The remaining two patients had midway lacerations which produced neither rupture nor aneurysmal formation. The midway LV lacerations are considered the result of LV incisions made at the time of mitral valve excision, generally in a setting where the left-sided cardiac chambers were only mildly dilated or normal and the tips of the blades of the scissors may have been inadequately visualized during mitral excision. This complication can be prevented by leaving the posterior mitral leaflet and its attached chordae intact or by applying exquisite care during the mitral excision procedure, or both. LV midway rupture may be most common cause of death early after MVR and operatively induced LV lacerations may lead to LV aneurysm late postoperatively.

Adult↗
PubMed1982

Sudden death in Prinzmetal's angina with coronary spasm documented by angiography. Analysis of three necropsy patients.

Clinical and necropsy findings are described in three patients who had angina pectoris at rest, S-T segment elevation on electrocardiography during chest pain, coronary arterial spasm on angiography and sudden death. Although significant "fixed" coronary narrowing (that is, narrowing due to atherosclerotic plaques) was appreciated by angiography in only one of the three patients, necropsy disclosed in all three patients severe fixed coronary narrowings involving particularly the artery in which spasm had been demonstrated during life. Additionally, examination of each 5-mm long segment of the coronary artery that had been spastic during life (two patients) disclosed several focally spastic segments at necropsy, indicating that spasm persisted after death. Although most previously described necropsy patients with Prinzmetal's angina had some fixed coronary narrowing, underlying fixed narrowing may be difficult to identify angiographically as demonstrated by the three patients in this study.

Adult↗
PubMed1982

Lipomatous hypertrophy of the interatrial septum: in vivo diagnosis.

Lipomatous hypertrophy of the interatrial septum (LHIS), a finding associated with obesity and advancing age, consists of the accumulation of adipose tissue, including fetal adipose tissue, in the interatrial septum cephalad and caudad to the fossa ovalis. Previous descriptions of this entity have been limited to autopsy examination. We report a patient in whom the diagnosis of LHIS was established during life by the use of computed tomographic cardiac imaging. As is often the case in patients discovered at autopsy to have LHIS, this patient had atrial fibrillation and, while in normal sinus rhythm, an abnormal P-wave morphology. This patient represents the first patient in whom the diagnosis of LHIS has been established during life. LHIS should be considered in the differential diagnosis of atrial fibrillation and other supraventricular rhythm/conduction disturbances, particularly in obese, elderly patients.

Aged↗
PubMed1982

Computed tomography in the diagnosis of pericardial heart disease.

To evaluate the use of computed tomography (CT) in the diagnosis of pericardial heart disease, 53 patients were prospectively studied by computed tomography of the chest and cardiac ultrasound. A diagnostic-quality CT study was done for all patients; a technically satisfactory ultrasound examination was not possible in six patients. Of 47 patients in whom both chest scans and satisfactory ultrasound studies were obtained, computed tomography showed pericardial thickening not shown by ultrasound in five patients. Estimated size of pericardial effusion was the same for both computed tomography and ultrasound. Computed tomography provided quantifiable evaluation of the composition of pericardial fluid in seven patients with either hemopericardium or purulent pericarditis. Neoplastic pericardial heart disease was detected by CT scan in four of the 53 patients. Computed tomography of the chest provides a sensitive evaluation of the pericardium and quality of pericardial effusion, and is a valuable adjunct in patients in whom cardiac ultrasound is technically unsatisfactory.

Adult↗
PubMed1981

Long-term clinical course of patients with normal coronary arteriography: follow-up study of 121 patients with normal or nearly normal coronary arteriograms.

To determine the long-term course of patients with normal coronary arteriograms, follow-up data regarding frequency of morbid cardiac events and extent of persistent clinical disability were obtained in 121 patients (72 women, 49 men; mean age 49 years) with normal (90%) or nearly normal (10%) coronary arteriograms. Mean length of follow-up was 4.3 years (range 1 to 11 years). Three (2.5%) patients died suddenly and unexpectedly. Four (3.4%) surviving patients suffered documented acute myocardial infarction (AMI) subsequent to initial arteriography. Three of seven patients who underwent repeat coronary arteriography were found to have disease in excess of that observed on initial arteriograms. The overwhelming majority (94% or 80%) of surviving patients continued to experience chest discomfort similar to that for which they underwent coronary arteriography and 75 (64%) continued to use antianginal drugs. Thus the finding of normal or nearly normal coronary arteriograms implies a highly favorable prognosis, although it does not establish immunity from a morbid cardiac event (AMI and/or sudden death); the likely basis for these events is progression of fixed obstructive disease, rather than coronary artery spasm or underestimation of extent of coronary disease by arteriography.

Acute Disease↗
PubMed1981

Lack of effect of aspirin on myocardial infarct size in the dog.

Pretreatment with platelet-inhibitory doses of aspirin (3 mg/kg body weight) has been shown to augment epicardial collateral flow by more than 50 percent (p less than 0.05) 4 hours after ligation of the left anterior descending coronary artery in dogs. To determine whether this favorable influence of aspirin is sufficient to decrease the amount of infarcted tissue, either intravenous aspirin, 3 mg/kg (n = 17), or saline solution (n = 17) was administered to dogs 10 minutes before occlusion of the left anterior descending coronary artery. Administration of saline solution or aspirin was repeated every 24 hours. By 72 hours, 5 dogs in each treatment group had died. Survivors were killed at 72 hours. The portion of the left ventricle at risk of infarction was delineated by perfusion of the aortic root with Evans blue and simultaneous perfusion of the distal left anterior descending coronary artery with saline solution under equal physiologic pressures. Slices of the stained heart were incubated with triphenyltetrazolium to identify gross infarct (with histologic confirmation). Total mass of left ventricle, myocardium at risk, and infarct size were measured in each dog. A direct relation was found between the mass at risk and the mass infarcted (r = 0.84, p less than 0.001). Aspirin-treated dogs did not differ from control dogs in percent ventricle at risk (mean +/- standard error 37 +/- 2 versus 40 +/- 2), percent infarct weight/left ventricle (29 +/- 3 versus 31 +/- 2) or percent infarct weight/weight of ventricle at risk (78 +/- 4 versus 77 +/- 3). Thus, despite aspirin's ability to inhibit platelet aggregation and to increase epicardial collateral flow by more than 50 percent, aspirin treatment failed to reduce infarct size in this dog model.

Animals↗
PubMed1981

Accuracy of angiographic determination of left main coronary arterial narrowing. Angiographic--histologic correlative analysis in 28 patients.

To evaluate the accuracy of coronary angiography in identifying severe narrowing of the left main coronary artery (LMCA), the degree of narrowing observed by angiography was compared to that observed at necropsy in 28 patients with symptomatic coronary heart disease in whom angiography had been performed within 40 days of death. The angiograms were evaluated independently by three experienced angiographers. In 20 of the 28 patients (71%), the degree of narrowing of the LMCA was either underestimated (13 patients) or overestimated (10 patients) by two or three of three angiographers; of 84 angiographic judgments made by the three angiographers in the 28 patients, 54 (64%) were underestimates (33 judgments, 39%) or overestimates (21 judgments, 25%) of the degree of LMCA narrowing. Of 12 LMCAs narrowed 76-100% in cross-sectional area at necropsy, six were underestimated at preoperative angiography by two or three of three angiographers; of 12 LMCAs narrowed 51-75% in cross-sectional area at necropsy, all 12 were either under- or overestimated angiographically by two or three of three angiographers; of four LMCAs narrowed 26-50% in cross-section at necropsy, two were overestimated by two of three angiographers. Thus, angiographic determination of degrees of narrowing of the LMCA during life is subject to considerable error. The angiographic errors appear to have resulted primarily from the presence of atherosclerotic plaque in the LMCA and an insufficient number of angiographic projections.

Adult↗
PubMed1980

Pseudoischemic "false positive" S-T segment changes induced by hyperventilation in patients with mitral valve prolapse.

Hyperventilation-induced S-T segment changes that simulate myocardial ischemia have previously been noted, but the origin of this electrocardiographic finding has never been defined. To investigate further the basis for this response, the records were reviewed of 1,678 consecutive patients who underwent forced hyperventilation for 90 seconds and treadmill exercise testing. Twenty-eight patients (1.7 percent) were identified in whom hyperventilation resulted in ischemic-appearing S-T segment changes, and follow-up was possible in 21 (17 women, 4 men). Of the 21 patients, 16 (76 percent), including 15 (88 percent) of the 17 women, had evidence of mitral valve prolapse, 6 on auscultation alone, 2 on echocardiography alone and 6 with a combination of studies. Ten of the 21 patients had a negative exercise test; of the 11 patients who had a positive exercise test, only 1 had angiographic evidence of coronary arterial narrowing. The finding of ischemic-appearing S-T segment changes in response to forced hyperventilation has a high predictive value for the presence of mitral valve prolapse, particularly in women. The possible association of autonomic factors and mitral valve prolapse in the pathogenesis of an abnormal response to hyperventilation is discussed.

Adult↗
PubMed1980

Comparison of amount of myocardial cell disorganization in operatively excised septectomy specimens with amount observed at necropsy in 18 patients with hypertrophic cardiomyopathy.

The extent of cardiac muscle cell disorganization in excised septectomy specimens in 18 patients was compared morphometrically with that observed at necropsy when these patients died after operation. Disorganization was present in all 18 patients at necropsy and was extensive (5 percent or greater) in 16 of the 18. In contrast, there was no disorganization in the operative specimens of three patients and only a trivial amount (less than 1 percent) in five others. Disorganization extensive enough (5 percent or greater) to suggest hypertrophic cardiomyopathy was present in the operative specimens of only 6 of the 18 patients. The mean (+/- standard error of the mean) area of disorganization at necropsy was 20 +/- 3 percent compared with 7 +/- 2 percent in the operative specimens (p less than 0.001). Thus, histologic examination of operatively excised septectomy specimens is of limited value in confirming the diagnosis of hypertrophic cardiomyopathy.

Adult↗
PubMed1980

Hemochromatosis heart disease: an unemphasized cause of potentially reversible restrictive cardiomyopathy.

Cardiac involvement in hemochromatosis typically results in congestive cardiomyopathy; a restrictive cardiomyopathy due to hemochromatosis is distinctly rare. A restrictive cardiomyopathy, which developed in the patient described in this report, was due to hemochromatosis which mimicked constrictive pericarditis clinically, echocardiographically and hemodynamically, and resulted in a thoracotomy for attempted surgical therapy. The fact that hemochromatosis represents the only cause of a restrictive cardiomyopathy that is potentially reversible by medical therapy makes early recognition of hemochromatosis heart disease important.

Cardiomyopathies↗
PubMed1980

Disseminated Petriellidium boydii and pacemaker endocarditis.

Clinical and morphologic findings are described in a 62 year old woman with "mixed connective tissue disease" who received corticosteroid therapy, and in whom disseminated and fatal Petriellidium boydii infection with right-sided endocarditis developed. The patient was a gardener. The organism is ubiquitous in soil in many part of the United States; therefore, it is likely that the infection was introduced by this means. Endocarditis due to P. boydii has not been reported previously. In the patient described, massive vegetations nearly obliterated the tricuspid valve orifice, encasing a pacemaker catheter which had been inserted eight years earlier. Although never previously isolated from blood cultures, P. boydii was isolated from 11 consecutive blood cultures. P. boydii is a true fungus and has only recently been appreciated as an opportunistic pathogen in a compromised host.

Endocarditis↗