Studies on the relation of the clinical manifestations of angina pectoris, coronary thrombosis, and myocardial infarction to the pathologic findings

Blumgart, Herrman L.; Schlesinger, M. J.; Davis, Donald W.

doi:10.1016/s0002-8703(40)90305-2

Cited by 552 publications

(74 citation statements)

References 18 publications

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“…Atheromas almost always lie beneath the ulceration, and the evolution of ulceration bears a histologic resemblance to rupture from within induced by an inflammatory foreign body response.4 The mechanism by which ulceration causes angina may be through release of vasoconstrictive compounds such as thromboxane A2 from platelets that aggregate at the site. 3 Platelet aggregation. Despite the fact that endothelial disruption causes platelet aggregation, we do not always see a thrombus attached to the ulceration either at angioscopy or at autopsy.…”

mentioning

confidence: 99%

A perspective of coronary disease seen through the arteries of living man.

Forrester¹,

Litvack²,

Grundfest³

et al. 1987

Circulation

192

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LONG DISPUTE," Voltaire (himself an incorrigible disputant) was fond of saying, "means both parties are wrong." Cardiology's longest debate concerns the pathogenesis of acute coronary disease. Today the resolution seems at hand: thrombus is once again the cause of acute infarction and thrombolysis is its cure. We do not wish to say, as Voltaire might, that this consensus is wrong, but it is incomplete because it leaves unanswered a crucial set of pathophysiologic questioins: What events precede coronary thrombosis?After formation of thrombus begins, are there fates other than infarction? At what points can the evolution of any of the acute (or chronic) coronary syndromes be arrested? Our Perspective proposes a systematic description-a paradigm-of the pathophysiology of acute and chronic coronary artery disease in man that deals specifically with these three questions.In the past year we have taken a metaphoric voyage through the coronary arteries of living man, using fiberoptic angioscopes. Through this exploration, we have seen the coronary endothelial surface in both acute and chronic coronary syndromes. Our unanticipated discovery has been that each of the common clinical presentations seems to have a specific, identifiable endothelial pathology. We will first describe

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mentioning

confidence: 99%

A perspective of coronary disease seen through the arteries of living man.

Forrester¹,

Litvack²,

Grundfest³

et al. 1987

Circulation

192

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“…The total occlusion in this patient was probably brought on by thromboembolic material, dislogded from the catheter into the preexisting high-degree stenosis. A parallel could be drawn between this case and noncatheter-induced, spontaneous infarction, since most autoptic studies seem to indicate acute thombotic occlusion of a high-degree lesion as the cause of myocardial infarction in the majority of patients (6,9,II,14). For this reason, it would seem plausible to try to limit myocardial injury in the early stages of spontaneous, evolving infarction by means of transluminal recanalization.…”

Section: Introductionmentioning

confidence: 68%

“…Most pathological findings seem to indicate that in the majority of cases, acute infarction is due to thrombotic obstruction or narrowing of high-degree atherosclerotic lesions (6,9,11,14). In this study the presence of thrombotic material at the site of acute coronary occlusion could be shown by means of coronary angiography in two patients for the first time.…”

Section: Spontaneous Recanalization In Medically Treated Patients (Grmentioning

confidence: 99%

“…In both patients there was collateral flow to the infarct area during the acute stage of infarction. A number of clinical (2 I, 32, 58), pathologic-anatomical (6,18) and experimental findings (45,48,53) indicate that the extent of myocardial injury can be limited by collateral flow. Therapy with nitrates and IABP could have been an additional factor limiting infarct size (5,7,12,17,20,25,31,33,34,43,50,51,56).…”

Section: Relationships Between Changes Of Local Wall Function and Cormentioning

confidence: 99%

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Initial experience with transluminal recanalization of the recently occluded infarct‐related coronary artery in acute myocardial infarction — Comparison with conventionally treated patients

Rentrop

Blanke

Karsch

et al. 1979

Clinical Cardiology

150

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In 7 patients, the recently occluded infarct‐related vessel was recanalized by transluminal catheter techniques during acute myocardial infarction (Group A). 4 patients had single‐vessel disease, 2 patients two‐vessels disease and one, involvement of three vessels. Control angiography was performed in 6 patients, 8 days to 7 months later. Changes of coronary artery anatomy and left ventricular function were compared with a group of 9 conventionally treated patients, who were found to have occlusion of the infarct‐related vessel in the acute stage (Group B). Five Group B patients had one‐vessel disease, 3 patients two‐vessel disease and 1 patient, involvement of all three vessels. In the chronic stage, all transluminally recanalized vessels were found to be patent in Group A. There was spontaneous recanalization of the infarct vessel in 4 of 9 Group B patients. In Group A, the length of the akinetic segment (AKS) decreased significantly (p < 0.05) from 145.4±48.5 mm to 73.2 ± 73.4 mm (mean ± SD). Volume parameters did not change significantly. In Group B, length of the AKS did not change significantly, EDVI increased significantly from 81.1 ±19.8 to 106.8±40.6 ml/m2 (p < 0.05); ESVI increased significantly from 41.7 ± 13.7 ml/m2 to 66.8 ± 37.9 ml/m2 (p < 0.01). In the acute stage, length of the AKS and volume parameters did not differ significantly between the two groups. In the chronic stage, AKS was significantly shorter (A: 73.2 ± 63.4 mm; 144.9 ± 59 mm (p < 0.0025)) and EF was significantly higher (A: 54.6 ±11.6%; B: 40.9 ±14.5% (p < 0.05)) in Group A. Peak CPK was lower in Group A (A: 1009 ± 827 U/l; B: 1324 ± 655 U/l), but this difference did not achieve statistical significance. Results of this pilot study suggest that transluminal recanalization in the early phases of acute myocardial infarction might result in limitation of myocardial injury. However, further research will be needed to improve the technique and to test its results.

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“…Clinical and cardiac morphologic observations in these AMI patients are summarized in table 1 26 of the 27 patients the ECG was either diagnostic or strongly suggestive of AMI. In all 27 patients, however, AMI was diagnosed clinically.…”

mentioning

confidence: 99%

Quantification of coronary arterial narrowing at necropsy in acute transmural myocardial infarction. Analysis and comparison of findings in 27 patients and 22 controls.

Roberts¹,

Jones²

1980

Circulation

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SUMMARY We quantitatively analyzed the degree and extent of coronary arterial narrowing by atherosclerotic plaques in the entire length of each of the four major coronary arteries in 27 necropsy patients with transmural acute myocardial infarction (AMI) and compared the findings with those in 22 control subjects. Of the 1403 5-mm segments examined in the 27 AMI patients, 484 (34%; controls 3%) were 76-100% narrowed in cross-sectional area by atherosclerotic plaques, 528 (38%; controls 25%) were 51-75% narrowed, 319 (23%; controls 44%) were 26-50% narrowed, and only 72 segments (5%; controls 28%) were 25% narrowed. 26 of the 27 patients the ECG was either diagnostic or strongly suggestive of AMI. In all 27 patients, however, AMI was diagnosed clinically. Death appeared to result from cardiogenic shock unassociated with cardiac rupture in 13 patients, from uncontrollable arrhythmias or conduction disturbances in five, from rupture of the left ventricular free wall in two and of the ventricular septum in three, from acute pulmonary edema not associated with shock in two, from intracerebral hemorrhage while on heparin therapy in one and from uncertain cause in one. The interval from onset of symptoms compatible with AMI to death ranged from 12 hours to 38 days (average 8 days), and was less than 24 hours in three patients and over 20 days in two. Except for two of the three patients who died during the first 24 hours after the onset of AMI, the infarcts were easily visible on gross inspection. The acute infarcts were transmural in all patients, defined as involvement of some portion of the inner half and all or portions of the outer half of the left ventricular wall.' In 19 of the 25 patients who had easily discernible infarct margins, the infarcts were large, involving more than 50% of a longitudinal dimension (i.e., from base to apex of left ventricle or involvement of more than one-third of the circumference of at least two of the six or seven ventricular slices cut at 1-cm intervals from apex to base parallel to the posterior atrioventricular sulcus). In the other six patients, the infarcts were of moderate size, involving 20-35% of the circumference of at least two ventricular slices or less than half of the longitudinal dimension of the left ventricle. No patient had a small infarct. At least two histologic sections extending from epicardium to endocardium and at least 2 cm wide from each patient were examined and the presence of coagulative type myocardial necrosis was confirmed in each by histologic examination. Patients

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Studies on the relation of the clinical manifestations of angina pectoris, coronary thrombosis, and myocardial infarction to the pathologic findings

Cited by 552 publications

References 18 publications

A perspective of coronary disease seen through the arteries of living man.

A perspective of coronary disease seen through the arteries of living man.

Initial experience with transluminal recanalization of the recently occluded infarct‐related coronary artery in acute myocardial infarction — Comparison with conventionally treated patients

Quantification of coronary arterial narrowing at necropsy in acute transmural myocardial infarction. Analysis and comparison of findings in 27 patients and 22 controls.

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