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Biomedical subjects

J T Fallon

Publications and source records attributed to J T Fallon.

At least 199 records · Page 11Linked to original sources
PubMed1981

Transluminal coronary angioplasty of postmortem human hearts.

Twelve autopsy human hearts were submitted to coronary angiography and coronary arterial balloon angioplasty. The effect of angioplasty was determined by follow-up coronary angiography as well as gross and microscopy inspection of the coronary arteries dilated. Fifty-four dilations were performed in 24 coronary arteries. Angiographically 50 of the 54 dilations resulted in a mean (+/- standard deviation) increase in luminal diameter ranging from 1.9 +/- 0.9 to 2.7 +/- 0.8 mm. Failure to increase luminal size was usually related to a predilation coronary diameter greater than that of the inflated angioplasty balloon. Dilation resulted in mural disruption with intimal or medial tears, or both, in 65 percent of arteries dilated. Disruption was more frequent in arteries with atherosclerosis and calcification. The mechanism of luminal enlargement in coronary angioplasty may be focal damage to the arterial wall with intimal or medial splitting as opposed to plaque compression as initially suggested.

Adolescent↗
PubMed1981

Nonsustained polymorphic ventricular tachycardia induced by electrical stimulation in 3 week old canine myocardial infarction.

To study the electrophysiology of ventricular tachycardia 3 to 4 weeks after myocardial infarction in a canine model, an anteroapical transmural infarct was created in 40 dogs by ligation of the left anterior descending coronary artery. An average of 25 days after myocardial infarction 32 dogs that survived the infarction and 4 control dogs with a sham operation underwent open chest electrophysiologic study. No ventricular arrhythmias could be induced by any mode of ventricular stimulation in any of the four control animals. Twenty-seven of 32 dogs with myocardial infarction had reproducible ventricular arrhythmias in response to ventricular stimulation. In 17 animals sustained uniform ventricular tachycardia could be reproducibly initiated by programmed ventricular stimulation. In another 10 dogs with myocardial infarction, the same modes of ventricular stimulation reproducibly initiated ventricular fibrillation. Seven of these 10 dogs also manifested reproducible nonsustained polymorphic ventricular tachycardia, characterized by beat to beat variation in QRS complex configuration and cycle length, in response to programmed ventricular stimulation. Nonsustained polymorphic ventricular tachycardia and sustained uniform ventricular tachycardia were rarely observed in the same dog and appeared to have different underlying mechanisms.

Animals↗
PubMed1981

Correlation of patterns of subendocardial reperfusion and left ventricular performance after ischemia.

Ninety-three dogs were studied with normothermic or hypothermic ischemia for 60 or 90 minutes, with or without potassium cardioplegia. Radioactive-labeled microspheres (9 +/- 1) were injected into the aortic perfusion cannula just prior to aortic cross-clamping and at 2, 6, and 10 minutes after the clamp was released. Left ventricular (LV) function was analyzed with a right heart bypass model before and 45 minutes after the ischemia period. Changes in LV function were defined as the arithmetic difference in the center of mass between preischemia and postischemia computer-drawn Sarnoff curves. Regardless of technique of myocardial protection, increased subendocardial flow 2 minutes after ischemia correlated strongly with preservation of LV function (p less than 0.01). Well-preserved hearts showed a rapid return to normal levels of coronary blood flow (p less than 0.01). In contrast, a delay in the peaking of subendocardial flow to 10 minutes was associated with poor function (p less than 0.01). There was a high correlation between ultrastructural morphology and LV function. While well-preserved hearts showed early preferential subendocardial perfusion, the poorly protected myocardium is unable to restore adequate subendocardial flow early in the reperfusion period.

Animals↗
PubMed1981

Ventricular septal rupture: a review of clinical and physiologic features and an analysis of survival.

Forty-one patients with postinfarction ventricular septal rupture were cared for in our hospital during 1971-1975. Cardiogenic shock developed after septal rupture in 55% of these patients. Shock was unrelated to site of infarction, extent of coronary artery disease, left ventricular ejection fraction, or pulmonary-to-systemic flow ratio, but mean pulmonary artery pressure was lower in shock than in nonshock patients. These observations suggest that shock was produced mainly by right ventricular impairment. Perioperative survival was much higher in patients who did not have shock preoperatively (14 of 17 [82+]) than in those who did (three of 11 [27%]). Magnitude of shunt, left ventricular ejection fraction, extent of coronary artery disease, and performance of aortocoronary bypass grafting were not distinctly correlated with perioperative survival. After a minimum 4-year follow-up, 76% of the perioperative survivors are alive, and none suffer more than New York Heart Association functional class II disability. All 13 unoperated patients (11 in shock) died within 3 months.

Aged↗
PubMed1980

Scanning electron microscopy after coronary transluminal angioplasty of normal canine coronary arteries.

Percutaneous coronary transluminal angioplasty is currently being proposed as a possible treatment for some patients with significant coronary arterial lesions. In this study scanning electron microscopy was used to assess the morphologic changes caused by the angioplasty balloon catheter in normal canine coronary arteries. Balloon inflation uniformly caused endothelial denudation with virtually immediate dense platelet adhesion to the subendothelial matrix. This platelet adhesion was unaffected by pretreatment with aspirin (35 mg/kg body weight) or heparin (2,000 units). However, intravenous administration of low molecular weight dextran almost completely prevented platelet adhesion to the exposed subendothelial connective tissues. It is concluded that even in normal canine coronary arteries (1) loss of endothelium is seen after transluminal angioplasty; (2) this endothelial damage stimulates platelet adhesion and thrombus formation; and (3) the immediate layering of platelets can be prevented by administration of low molecular weight dextran.

Animals↗
PubMed1980

Transluminal angioplasty: correlation of morphologic and angiographic findings in an experimental model.

The morphologic consequences of transluminal angioplasty of stenotic atherosclerotic coronary arteries are unknown. This study describes the production of aortoiliac atherosclerosis in rabbits and reports the morphologic changes after transluminal angioplasty of stenotic arterial lesions. Atherosclerotic lesions were evaluated angiographically before and after transluminal angioplasty and were studied histologically and by electron microscopy after angioplasty. Moderatley stenotic aortic segments showed denudation of endothelial cells and deposition of a carpet of platelets enmeshed in fibrin. Medial and intimal compression were not seen. Intimal plaque disruption and splitting of atheromatous plaques were observed in more stenotic vessels where dilatation during angioplasty is relatively greater. Transluminal angioplasty, therefore, acutely causes desquamation of endothelial cells and superficial plaque elements, splitting of atheroma and subsequent deposition of platelets and fibrin in the area of angioplasty. This experimental model may be useful to evaluate the morphologic changes after angioplasty and might be used in further studies to determine the long-term pathophysiologic changes after transluminal angioplasty.

Animals↗
PubMed1980

Sustained ventricular tachycardia in recent canine myocardial infarction.

To study recurrent ventricular tachycardia in the late phase or myocardial infarction (MI), transmural anteroapical infarcts were created by ligation of the left anterior descending (LAD) coronary artery in 25 dogs. Twenty dogs survived LAD ligation and underwent an open-chest electrophysiologic study an average of 20 days after MI. Programmed electrical stimulation was carried out using the extrastimulus technique and short bursts of rapid ventricular pacing via bipolar electrodes positioned at multiple left ventricular endocardial sites. Sixteen dogs had electrically induced ventricular tachycardia, and in 11, sustained ventricular tachycardia was reproducibly initiated and terminated by programmed ventricular stimulation. Short bursts of rapid left ventricular pacing from areas in periinfarct zone was the most effective technique for initiating ventricular tachycardia. The electrophysiologic phenomena in this model of sustained ventricular tachycardia in 3-week-old MI included electrically induced changes in rate and morphology and biventricular capture without termination during tachycardia.

Animals↗
PubMed1980

Experimental angioplasty: lessons from the laboratory.

To elucidate the pathophysiologic mechanisms of transluminal angioplasty, normal coronary arteries in dogs, atherosclerotic human coronary arteries, and atherosclerotic vessels in rabbits were studied after angioplasty. Normal canine coronary arteries showed desquamation of endothelium, exposure of subendothelial connective tissue elements, and deposition of a carpet of platelets, fibrin, and occasional red blood cells. Administration of low molecular weight dextran before angioplasty decreased platelet deposition. Atherosclerotic human coronary arteries studied postmortem showed enlargement of lumen size after angioplasty due to splitting and disruption of the plaque and the underlying media. Endothelial desquamation and splitting of the plaque were also seen in atherosclerotic vessels in rabbits after angioplasty. The amount of splitting seems to depend on the relative size of the stenotic vessel and the inflated angioplasty balloon. Animals studied sequentially showed retraction of the separated intimal plaque elements and further lumen enlargement after 1-2 weeks. Two mechanisms of successful angioplasty are suggested by these studies: (1) desquamation of superficial plaque elements and (2) splitting of the plaque with retraction of intimal flaps as healing occurs. These mechanisms have important implications for the treatment of patients undergoing percutaneous transluminal angioplasty.

Animals↗
PubMed1980

Pathology of arterial lesions amenable to percutaneous transluminal angioplasty.

Percutaneous transluminal angioplasty is rapidly becoming an accepted therapeutic method for stenotic arterial disease. Atherosclerotic lesions of the coronary, renal, and peripheral arteries are favorable stenoses for angioplasty because of their generally focal nature, proximal location, and pathologic features. Other types of arterial stenoses may also be amenable to transluminal angioplasty, including fibromuscular dysplasia, Takayasu arteritis, and congenital coarctation, by virtue of their localized nature and pathologic features similar to atherosclerotic lesions. Although the mechanism of successful angioplasty is poorly understood, disruption of intimal atherosclerotic lesions apparently occurs and is often responsible for the increase in luminal diameter seen angiographically. The potential complications of this procedure include dissection, rupture, thrombotic occlusion, acceleration of the atherosclerotic process, and distal embolization of plaque debris.

Aortic Coarctation↗
PubMed1979

Protection by plasma proteins of the isolated lamb heart perfused with stroma-free hemoglobin at 38 degrees.

Isolated lamb hearts were perfused for eight hours at 38 degrees with stroma-free hemoglobin solution (SFHS). The preservation of cardiac structure and function was studied. Control hearts perfused with blood (N = 6) developed no ventricular failure or significant weight gain (13% +/- 5), showed no alteration of cellular ultrastructure, and little interstitial edema. Hearts perfused with 7% (N = 7) or 11% (N = 5) SFHS contracted less well, became edematous (22% and 44% weight gain) and showed altered mitochondria, capillary endothelial swelling and hemoglobin extravasation into the interstitial space. The addition of 5-7% albumin to SFHS (N = 9) markedly reduced interstitial edema (weight gain 11% +/- 13), preserved mitochondria, prevented endothelial swelling, and limited transcapillary escape of hemoglobin. Thus isolated hearts perfused with SFHS develop vascular endothelial damage and an increase in capillary permeability. The addition of plasma proteins to the perfusate protects against this injury.

Animals↗
PubMed1979

Cardiomyopathic syndrome caused by coronary artery disease. III: Prospective clinicopathological study of its prevalence among patients with clinically unexplained chronic heart failure.

Each day, for one year, the medical records of adult patients who died in hospital were reviewed before seeing the necropsy findings. For those patients who had had chronic left or left and right heart failure, a presumptive cause was assigned on the basis of antemortem clinical data. Of 740 consecutive patients who were studied at necropsy, 90 had had chronic heart failure. In 15 patients the cause of heart failure was not apparent by clinical criteria; of these, 7 were found at necropsy to have cardiomyopathic syndrome caused by coronary artery disease. In retrospect, the presence of overt diabetes mellitus was a clue that cardiomyopathy caused by coronary artery disease was the cause of clinically unexplained heart failure; 5 of 7 patients with unexplained heart failure who were found to have this at necropsy were diabetic, whereas only 1 of the other 8 patients with clinically unexplained heart failure was diabetic (P less than 0.05). Patients in whom clinically unexplained heart failure was found to be the result of cardiomyopathy caused by coronary artery disease had multiple myocardial infarctions on pathological examination, which, with one exception, were nontransmural. By contrast, myocardial infarctions were transmural on pathological examination in each of 7 matched 'controls' with heart failure, in whom the diagnosis of coronary artery disease had been clinically apparent (P less than 0.01).

Adult↗