Biomedical subjects

N Kantrowitz

Publications and source records attributed to N Kantrowitz.

5 recordsLinked to original sources

PubMed1997

Thrombin Generation and Activity During Coronary Angioplasty: Influence of Angiographic Lesion Morphology.

OBJECTIVE: To investigate the relationships between coronary atherosclerotic plaque injury, lesion morphology, and activation of the coagulation cascade. BACKGROUND: Balloon angioplasty of coronary lesions may result in intracoronary thrombin generation and activity. It is unknown whether the angiographic morphology of the lesion prior to intervention, an indicator of the presence of thrombus in the lesion, is a determinant of the degree of coagulation cascade activation. METHODS AND RESULTS: Biochemical markers of thrombin generation (prothrombin fragment F1+2) and thrombin activity (fibrinopeptide A; FPA) were measured in coronary blood before, 1 and 10 minutes after percutaneous transluminal coronary angioplasty (PTCA) in 24 patients with an angiographically complex lesion morphology and 24 patients with an angiographically simple lesion morphology. Using previously defined criteria, 18 of the 48 patients (38%) demonstrated a significant rise in coronary plasma F1+2; 8 of these 18 (44%) had simple and 10 of 18 (55%) had complex angiographic lesion morphologies (p=NS). With respect to thrombin activity, 15 of the 48 patients (31%) demonstrated a significant rise in coronary plasma FPA; 7 of these 15 patients (47%) had a simple lesion morphology and 8 (53%) had a complex morphology (p=NS). When analyzed as a group, patients with complex lesion morphologies demonstrated a small elevation in coronary plasma levels of FPA 10 minutes post-PTCA (median 3.2 ng/ml, 95% CI 2.4Ð5.8 ng/ml) in comparison to the levels measured proximal to the lesion pre-PTCA (median 2.1 ng/ml, 95% CI 1.6Ð3.5 ng/ml; p=0.05). In contrast, in the group of patients with simple lesion morphologies, the plasma FPA levels proximal to the lesion pre-PTCA (median 2.1 ng/ml, 95% CI 1.5 to 3.9 ng/ml) were similar to those measured 10 minutes after the procedure (median 2.0 ng/ml, 95% CI 1.5 to 6.3 ng/ml; p=NS). CONCLUSIONS: In comparison to patients with angiographically complex lesions, patients with angiographically simple lesions demonstrate a similar incidence (~33%) of elevated coronary plasma thrombin generation (F1+2) and activity (FPA) after PTCA. As a group, patients with angiographically complex lesions (irregular borders, overhanging edges, filling defects) demonstrate a slightly greater increase in thrombin activity in comparison to patients with simple lesion morphologies. Percutaneous coronary interventions of lesions with a wide variety of angiographic morphologies are prone to result in activation of the coagulation cascade.

Journal Article↗

PubMed1991

Neutrophil-endothelial cell interaction in critical illness.

Sepsis syndrome frequently results in endothelial injury in many organ systems. To evaluate neutrophil-pulmonary endothelial cell interaction in the sepsis syndrome, we studied 39 critically ill patients prospectively and 20 normal volunteers. Thirteen patients with sepsis (mean age, 71.4 years), 14 patients in an intensive care unit control group (mean age 65.4 years), and 12 patients admitted with acute myocardial infarction (mean age, 66.8 years) were evaluated. Blood samples were drawn from septic patients within 24 hours and from ICU and MI patients within 72 hours of admission. All sepsis patients were culture positive, 6 of 13 from the blood. Both renal failure and ARDS developed in 54 percent of septic patients. 51Cr-labelled neutrophils were prepared and added to bovine pulmonary endothelial cell monolayers with and without added phorbol myristate acetate. Endothelial cells with adherent PMA and nonadherent PMN's, were harvested and radioactivity in each fraction measured with a gamma scintillation counter. Baseline and maximally stimulated (PMA, 3.0 ng/ml) neutrophil adherence to endothelial cells were similar in all patients groups. However, in septic patients, PMA-stimulated PMN adherence was reduced at lower doses, most significantly in those who developed ARDS within 24 to 48 hours of admission (p less than 0.05). Seventy-one percent of patients who developed ARDS had reduced stimulated adherence (PMA 1.0 ng/ml) compared to 22 percent of critically ill patients who did not. We conclude that diminished adherence of neutrophils to endothelium in response to low-level PMA stimulation is significantly more common in patients with sepsis who develop ARDS. Our findings suggest that PMN-endothelial cell interaction is altered by the time sepsis is clinically recognized but before the development of ARDS. We speculate that the observed reduction in adherence of the PMN to endothelial cells may be a consequence of down-regulation by mediators generated in the inflammatory response to sepsis and/or the need for active participation of septic endothelium in this interaction.

Aged↗

PubMed1989

Effects of intravenous metoprolol on global and regional left ventricular function after coronary arterial reperfusion in acute myocardial infarction.

Coronary reperfusion in myocardial infarction improves infarct zone motion, but its effect on the global ejection fraction has been less consistent. The directional movement of the ejection fraction is determined by the opposing influences of improved infarct zone motion and diminishing hyperkinesia in the noninfarct zone. Noninfarct zone hyperkinesia has been attributed to catecholamine stimulation, the Frank-Starling mechanism or intraventricular interactions that unload noninfarcted segments. To investigate the influence of catecholamine stimulation, 9 men presenting with a first myocardial infarction (mean age 53 +/- 13 years) were studied. Coronary reperfusion was accomplished less than 4 hours after the onset of myocardial infarction. Radionuclide ventriculography was then performed before and immediately after the intravenous administration of 15 mg of metoprolol. End-diastolic volume did not change, but end-systolic volume increased 28% after metoprolol (p = 0.041). The ejection fraction decreased from 55 +/- 13% before metoprolol to 45 +/- 14% after its administration (p = 0.002). There was no effect of intravenous metoprolol on infarct zone motion, whereas motion in the noninfarcted segment decreased (p = 0.002). The patients underwent repeat ventriculography after receiving metoprolol, 100 mg orally twice a day for 9 days. Infarct zone motion improved (p less than 0.002) and the ejection fraction increased to 55 +/- 12% (p less than 0.02). Normal zone motion did not change. Thus, compensatory hyperkinesia is at least in part caused by catecholamine stimulation. Conclusions regarding the effects of reperfusion on global ventricular performance can be influenced by the timing of ejection fraction determinations relative to metoprolol therapy.

Adult↗

PubMed1985

A new method for assessing right-sided heart pressures using encapsulated microbubbles--a preliminary report.

A new noncatheter method for measuring pressures of the right side of the heart uses specially manufactured microbubbles of carbon dioxide injected into the peripheral venous system. Sudden expansion of these bubbles in the cardiac chambers causes bubble oscillations at a frequency that is primarily a function of surrounding pressure. The oscillations are recordable by a microphone on the chest wall. The preliminary experience has been in dogs and further development is needed before we can begin clinical testing of the method. In its current form, the potential for measuring higher systolic pressures seems better than that for lower diastolic pressures.

Animals↗

PubMed1981

Histamine provocation of clinical coronary artery spasm: implications concerning pathogenesis of variant angina pectoris.

Twelve patients with nonexertional chest pain and nonobstructive fixed coronary disease (less than 50% luminal diameter narrowing) were given histamine to investigate the potential role (coronary artery H1 receptor agonism) of the endogenous agent in producing coronary artery spasm (CAS). Histamine, at intravenous dose of 0.5 to 1.0 microgram/kg/min, provoked CAS in four patients. In six patients neither histamine nor ergonovine provoked spasm, and these patients were considered by chronic follow-up evaluation to have noncardiac etiology for their chest pain syndrome. In one patient CAS was provoked with ergonovine but not by histamine, and one ergonovine-positive patient had an equivocally positive histamine result. Pretreatment with cimetidine (H2 receptor antagonism) was necessary to avoid unpleasant side effects of histamine. Thus these observations indicate that histamine should be included among the specific agents capable of inducing CAS and provide new insight concerning the mechanism(s) causing variant angina pectoris.

Adult↗