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Biomedical subjects

R Gorlin

Publications and source records attributed to R Gorlin.

At least 55 records · Page 3Linked to original sources
PubMed1988

Angiographic demonstration of a common link between unstable angina pectoris and non-Q-wave acute myocardial infarction.

The coronary morphology of ischemia-related arteries in unstable angina and Q-wave acute myocardial infarction (AMI) has been described. An eccentric stenosis with overhanging edges or irregular borders (type II eccentric) was seen in most lesions less than 100% occluded and probably represented plaque disruption, nonocclusive thrombus or both. The coronary morphology of non-Q AMI has not been described. Thus, the angiograms of 106 consecutive patients catheterized with either unstable angina (n = 73) or non-Q AMI (n = 33) and an identifiable ischemia-related artery were prospectively analyzed. Non-Q AMI was diagnosed by prolonged chest pain and new and persistent ST-T changes or creatine phosphokinase twice the normal level. The results showed a higher incidence of total occlusion of the ischemia-related artery in non-Q AMI (21%) compared with unstable angina (8%) (p = 0.1). The coronary morphology of nonoccluded ischemia-related arteries was similar with preponderance of type II eccentric lesions in both unstable angina and non-Q AMI. These lesions were found in 65% of ischemia-related arteries in non-Q AMI but were uncommon (3%) in nonischemia-related arteries with significant (50% to 100%) stenoses. Therefore, the type II eccentric lesion is a sensitive and specific marker of less than 100% occluded ischemia-related arteries in both unstable angina and non-Q AMI. These similarities in coronary morphology suggest a similar pathogenesis, which, as previously suggested, may relate to plaque disruption with or without thrombus. Unstable angina and non-Q AMI appear to represent part of a continuous spectrum of acute coronary artery disease. Further, the management of patients with non-Q AMI should be similar to patients with unstable angina and possibly include anticoagulation and consideration for early catheterization.

Aged↗
PubMed1988

Angiographic progression of coronary artery disease and the development of myocardial infarction.

There are few data on angiographic coronary artery anatomy in patients whose coronary artery disease progresses to myocardial infarction. In this retrospective analysis, progression of coronary artery disease between two cardiac catheterization procedures is described in 38 patients: 23 patients (Group I) who had a myocardial infarction between the two studies and 15 patients (Group II) who presented with one or more new total occlusions at the second study without sustaining an intervening infarction. In Group I the median percent stenosis on the initial angiogram of the artery related to the infarct at restudy was significantly less than the median percent stenosis of lesions that subsequently were the site of a new total occlusion in Group II (48 versus 73.5%, p less than 0.05). In the infarct-related artery in Group I, only 5 (22%) of 23 lesions were initially greater than 70%, whereas in Group II, 11 (61%) of 18 lesions that progressed to total occlusion were initially greater than 70% (p less than 0.01). In Group I, patients who developed a Q wave infarction had less severe narrowing at initial angiography in the subsequent infarct-related artery (34%) than did patients who developed a non-Q wave infarction (80%) (p less than 0.05). Univariate and multivariate analysis of angiographic and clinical characteristics present at initial angiography in Group I revealed proximal lesion location as the only significant predictor of evolution of lesions greater than or equal to 50% to infarction. This retrospective study suggests that myocardial infarction frequently develops from previously nonsevere lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Reversal of chronic ischemic myocardial dysfunction after transluminal coronary angioplasty.

From a cohort of patients referred for elective transluminal coronary angioplasty, a subset of patients was evaluated to determine whether revascularization using coronary angioplasty could salvage chronically ischemic myocardium. Reversible chronic ischemic left ventricular dysfunction was identified by a severe wall motion abnormality at rest and at least one of the following: 1) persistent angina pectoris; 2) postextrasystolic ventricular contraction potentiation of motion in the asynergic zone on baseline ventriculogram; and 3) thallium-201 uptake in the asynergic zone. Twelve patients were identified as having reversible chronic ischemia and underwent coronary angioplasty. Their mean age was 63 +/- 11 years and duration of symptoms 8.3 +/- 9.7 weeks. Immediate pre- and postangioplasty left ventriculograms were obtained. Regional wall motion was analyzed using a radial axis model, and global ejection fraction was calculated. After angioplasty, tension development (heart rate-systolic pressure product) increased in the absence of an increase in left ventricular end-diastolic pressure. Global ejection fraction increased from 46 +/- 20 to 62 +/- 19% (p less than 0.005). The percent of left ventricular diastolic perimeter showing asynergy decreased from 29 +/- 11 to 10 +/- 13% (p less than 0.005). During follow-up ranging from 6 to 51 months, sudden death occurred in one patient who had had no improvement in wall motion after angioplasty, repeat angioplasty was performed in three patients and eight patients remained asymptomatic. Application of easily obtainable clinical data identifies a subset of patients with chronically ischemic myocardium. Coronary angioplasty in such patients is useful in salvaging hibernating myocardium.

Adult↗
PubMed1988

The biological actions and potential clinical significance of dietary omega-3 fatty acids.

The exploration of the effects of fish oil in cardiovascular disease and inflammation seems to be a promising avenue of research. There is evidence indicating the role of marine oils in inhibiting coagulation and platelet, leukocyte, and T-lymphocyte function. Moderate amounts of fish oil reduce serum triglyceride and very-low-density lipoprotein levels, while effects on cholesterol, high-density lipoprotein, and low-density lipoprotein levels are unpredictable except at extremely large doses. Putative actions in lowering blood pressure and limiting myocardial infarct size require further study. The clinician needs to be aware of the dose- and time-dependent nature of the measurable effects of fish oil. The folly of recommending two to four capsules per day is contrasted with the ten to 30 capsules required to produce a specific desired effect.

Animals↗
PubMed1987

Quantitative and qualitative effects of intracoronary streptokinase in unstable angina and non-Q wave infarction.

Thrombolytic therapy has been shown to be effective in reopening totally occluded arteries in acute myocardial infarction. Coronary thrombus is also believed to play a role in the pathophysiology of unstable angina and non-Q wave infarction. However, few patients with these two acute coronary syndromes have been treated with intracoronary streptokinase. Therefore, 100,000 to 300,000 IU (mean 177,000 +/- 80,000 IU) of intracoronary streptokinase was infused into 36 consecutive catheterized patients who either presented with an acute episode of unstable angina or had had a recent non-Q wave infarction and in whom a less than 100% occluded ischemia-producing artery could be identified. Qualitative techniques utilizing vessel magnification and quantitative analysis with digital subtraction were performed on the ischemia-producing coronary lesion before and immediately after streptokinase therapy and 3 to 10 days later in 18 patients who were restudied at the time of transluminal coronary angioplasty. Before streptokinase treatment, 24 (67%) of 36 ischemia-producing arteries contained eccentric, irregular lesions. The percent diameter stenosis and percent area stenosis in all ischemia-producing arteries averaged 83.8 +/- 8.3% and 94.8 +/- 3.3%, respectively. After streptokinase treatment there were 23 arteries (64%) with eccentric irregular lesions. The percent diameter stenosis and percent area stenosis in all ischemia-producing arteries were similar to pre-streptokinase values (82.9 +/- 5.9% and 93.8 +/- 4.0%, respectively). At restudy, there were also no significant changes in any quantitative or qualitative variable. Five individual patients showed a significant reduction in percent stenosis after streptokinase. This improvement was independent of duration of symptoms, use of heparin before angiography, streptokinase dose or reduction of fibrinogen levels post-streptokinase. Two additional patients deteriorated clinically and developed total occlusion of the ischemia-producing artery within 12 hours of streptokinase infusion. These data suggest that intracoronary streptokinase may be of limited utility in either unstable angina or recent non-Q wave infarction with a less than 100% occluded ischemia-producing artery. In these syndromes, thrombus may be organized or short infusions may be given too late to be effective. In some cases, thrombus may even be absent. Whether longer infusion of streptokinase or other thrombolytic agents will be of benefit remains to be determined.

Adult↗
PubMed1987

Doppler echocardiographic analysis of left ventricular filling in treated hypertensive patients.

Early detection and prevention of cardiac dysfunction is an important goal in the management of hypertensive patients. In this study, Doppler echocardiography was used to evaluate the pattern of left ventricular diastolic filling in 38 subjects: 18 treated hypertensive patients (blood pressure 141 +/- 17/83 +/- 10 mm Hg, mean +/- SD) without other coronary risk factors and 20 risk-free normotensive subjects of similar age (47 +/- 10 and 49 +/- 13 years, respectively). Peak velocity of late left ventricular filling due to the atrial contraction was greater in hypertensive compared with normotensive subjects (69 +/- 14 versus 52 +/- 13 cm/s; p less than 0.001). Peak velocity of late filling was significantly greater in hypertensive versus normotensive subjects in those aged 50 years or younger and those older than age 50 (65 +/- 12 versus 50 +/- 11; p less than 0.01 and 75 +/- 15 versus 56 +/- 15 cm/s; p less than 0.05, respectively). In hypertensive subjects, peak velocity of late filling did not correlate with routine indexes of hypertensive heart disease (including posterior wall thickness and left ventricular mass), systolic and diastolic blood pressure or duration of hypertension. These results indicate that increased velocity of late left ventricular filling may be independent of left ventricular hypertrophy and persist despite effective blood pressure control.

Adult↗
PubMed1987

Atrial kinetics and left ventricular diastolic filling in the healthy elderly.

A delay of left ventricular isovolumic relaxation and decrease in myocardial compliance may result in a decline of measured early filling rates in elderly subjects. Previous studies of diastolic function, however, have not excluded coronary artery disease or addressed the contribution of atrial contraction to diastole. The present study evaluated radionuclide-derived diastolic variables in 13 healthy elderly volunteers aged 75 +/- 6 years without symptoms or risk factors for coronary disease who had normal findings on the stress electrocardiogram, stress gated blood pool imaging and two-dimensional echocardiogram. Results were compared with those of a group of 10 healthy young volunteers aged 26 +/- 5 years. High count, 32 frame, double-buffered gated blood pool acquisitions were obtained at rest in the left anterior oblique view with an RR interval variation less than 5%. Left ventricular time-activity curves were analyzed and flow-volume loops for each group were constructed. In the healthy elderly: peak early diastolic filling rate is decreased, time of peak early filling and time to first third of diastolic filling are delayed, and peak late left ventricular filling rate and percent of atrial filling volume are augmented, suggesting an adaptive response of the atria to diminished left ventricular compliance.

Aged↗
PubMed1986

Angiographic evolution of coronary artery morphology in unstable angina.

As previously reported in acute presentations of unstable angina, an identifiable characteristic coronary artery lesion has been found in about 70% of cases at coronary arteriography. This takes the form of an eccentrically placed convex stenosis with a narrow neck due to one or more overhanging edges or irregular, scalloped borders, or both. To study the evolution of lesions responsible for unstable angina, coronary artery anatomy and morphology on angiography were evaluated in patients with stable angina progressing to unstable angina. Group I comprised 25 patients with a history of stable angina who were restudied after an acute episode of unstable angina and Group II comprised 21 patients with little or no change in symptoms between catheterizations. Progression of coronary disease occurred in 19 (76%) of 25 patients in Group I compared with 7 (33%) of 21 in Group II (p less than 0.001). Of the 25 lesions with progression in Group I, 17 progressed to less than 100% and 8 to 100% occlusion. Eighteen of these 25 lesions in Group I were previously insignificant (less than 50% occlusion on the first catheterization). In contrast, of the eight lesions with disease progression in Group II, only two were previously insignificant while six showed at least 50% occlusion on the initial study. The eccentric lesion was seen in 71% of all lesions with progression to less than 100% occlusion in Group I, but it was not seen in any Group II vessel with progression.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Coronary angiographic morphology in myocardial infarction: a link between the pathogenesis of unstable angina and myocardial infarction.

It has previously been shown that analysis of coronary morphology can separate unstable from stable angina. An eccentric stenosis with a narrow neck or irregular borders, or both, is very common in patients who present with acute unstable angina, whereas it is rare in patients with stable angina. To extend these observations to myocardial infarction, the coronary morphology of 41 patients with acute or recent infarction and nontotally occluded infarct vessels was studied. For all patients, 27 (66%) of 41 infarct vessels contained this eccentric narrowing, whereas only 2 (11%) of 18 noninfarct vessels with narrowing of 50 to less than 100% had this lesion (p less than 0.001). In addition, a separate group of patients with acute myocardial infarction who underwent intracoronary streptokinase infusion were also analyzed in similar fashion. Fourteen (61%) of 23 infarct vessels contained this lesion after streptokinase infusion compared with 1 (9%) of 11 noninfarct vessels with narrowing of 50 to less than 100% (p less than 0.01). Therefore, an eccentric coronary stenosis with a narrow neck or irregular borders, or both, is the most common morphologic feature on angiography in both acute and recent infarction as well as unstable angina. This lesion probably represents either a disrupted atherosclerotic plaque or a partially occlusive or lysed thrombus, or both. The predominance of this morphology in both unstable angina and acute infarction suggests a possible link between these two conditions. Unstable angina and myocardial infarction may form a continuous spectrum with the clinical outcome dependent on the subsequent change in coronary supply relative to myocardial demand.

Angina Pectoris↗
PubMed1985

Angiographic morphology and the pathogenesis of unstable angina pectoris.

In 110 patients with either stable or unstable angina, the morphology of coronary artery lesions was qualitatively assessed at angiography. Each obstruction reducing the luminal diameter of the vessel by 50% or greater was categorized into one of the following morphologic groups: concentric (symmetric narrowing); type I eccentric (asymmetric narrowing with smooth borders and a broad neck); type II eccentric (asymmetric with a narrow neck or irregular borders, or both); and multiple irregular coronary narrowings in series. For the entire group, type II eccentric lesions were significantly more frequent in the 63 patients with unstable angina (p less than 0.001), whereas concentric and type I eccentric lesions were seen more frequently in the 47 patients with stable angina (p less than 0.05). Type II eccentric lesions were also present in 29 of 41 arteries in patients with unstable angina compared with 4 of 25 arteries in those with stable angina (p less than 0.0001) in whom an "angina-producing" artery could be identified. Therefore, type II eccentric lesions are frequent in patients with unstable angina and probably represent ruptured atherosclerotic plaques or partially occlusive thrombi, or both. A temporary decrease in coronary perfusion secondary to these plaques with or without superimposed transient platelet thrombi or altered vasomotor tone may be responsible for chest pain in some of these patients with unstable angina.

Angina Pectoris↗