Toshiro Kurosawa

Polymorphisms in the platelet-endothelial cell adhesion molecule-1 (PECAM-1) gene, Asn563Ser and Gly670Arg, associated with myocardial infarction in the Japanese.

Abstract: We examined three missense polymorphisms of platelet‐endothelial cell adhesion molecule‐1 (PECAM‐1), Val125Leu, Asn563Ser, and Gly670Arg, in 136 Japanese patients with myocardial infarction and 235 healthy Japanese controls. We found that these polymorphisms were in linkage disequilibrium with each other and that frequencies of 125Leu, 563Ser, and 670Arg alleles were significantly increased in patients compared with controls (0.522 vs 0.447, p= 0.048; 0.585 vs 0.502, p= 0.030; and 0.577 vs 0.492, p= 0.032, respectively). The frequencies of homozygotes for 563Ser and 670Arg alleles were also significantly increased in the patients (33.1% vs 23.4%, odds risk [OR] = 1.62, p= 0.040, 95% confidence interval [95%CI] = 1.01‐2.58; and 32.4% vs 23.0%, OR = 1.60, p= 0.048, 95%CI = 1.00‐2.57, respectively). These observations suggest that the 563Ser/Ser genotype and 670Arg/Arg genotype of PECAM‐1 are novel genetic risk factors of myocardial infarction in Japanese. Stratification analysis of the patients showed that the associations of these PECAM‐1 genotypes with myocardial infarction were preferentially found in male and younger patients (age of onset of myocardial infarction less than 60 years). In addition, the associations were stronger in patients with three‐vessel disease than in the others and appeared independent of conventional risk factors including smoking, hypertension, diabetes mellitus, hyperlipidemia, and obesity.

Long.term follow-up of coronary artery dissection due to blunt chest trauma with spontaneous healing in a young woman

We report a previously healthy 17-year-old woman who experienced coronary artery dissection with an acute transmural anterior myocardial infarction and myocardial contusion following blunt chest trauma in a motorcycle accident. A chest roentgenogram on admission was normal, and an electrocardiogram showed an acute transmural anterior myocardial infarction with complete right-bundle-branch block. A 2D echocardiogram revealed an akinesis of the anterior wall and a hypokinesis of the posterior wall in the left ventricle. Initial coronary angiography demonstrated severe stenosis with delayed antegrade filling in the proximal left anterior descending artery. Technetium-99m pyrophosphate myocardial scintigraphy demonstrated diffuse tracer uptake in the left ventricular wall. Follow-up coronary angiography performed 1 year after the accident showed a minor stenosis without any filling defects. We describe long-term follow-up of the coronary artery dissection following blunt chest trauma with spontaneous healing.

Atrial Natriuretic Peptide in Human Urine

SummaryA highly sensitive radioimmunoassay to measure atrial natriuretic peptide (ANP) concentration in urine has been established, and its clinical usefulness is presented. ANP in urine was stable at 4° C for several days and was easily measured by our radioimmunoassay. The average ANP excretion in 65 healthy persons was 25.0±1.4 ng/day (mean ± SEM) and the fractional excretion of ANP was 0.7±0.05%. In 14 patients with congestive heart failure, the average ANP excretion was 119.2±29.4 ng/day, which decreased to 53.3±11.0 after successful treatment.

Changes of molecular forms of atrial natriuretic peptide after treatment for congestive heart failure

SummaryIn the present study, an attempt was made to clarify whether ANP molecular forms in the plasma of severe congestive heart failure patients differ from those in healthy persons and whether ANP molecular forms in the plasma of the patients were changed by successful treatment of cardiac disease.Twenty patients with congestive heart failure were treated at Kitasato University Hospital. They were classified as class III or IV by New York Heart Association criteria at the time of admission. Plasma ANP concentrations decreased after treatment from 356 ± 58.2 to 72.3 ± 14.8 pg/ml. The gel permeation chromatograms from the plasma of healthy persons showed low, or low and high molecular weight ANP peaks which correspond to the elution positions of authentic α-ANP or ribonuclease A (mol.wt., 13.7 kdalton). In patients with severe congestive heart failure at a severe stage, middle molecular weight ANP consisted with the elution position of authenticβ-ANP was particularly noted in addition of low and high molecular weight ANP peaks. This middle molecular weight peak disappears in most of cases by successful treatment. Molecular forms in the plasma obtained from the coronary sinus and the inferior or superior vena cava were essentially the same.These results indicate that the middle molecular weight ANP supposed asβ-ANP may particularly be secreted in severe congestive heart failure patients.

Atrial natriuretic peptide is only a minor diuretic factor in dehydrated subjects immersed to the neck in water

SummaryTo determine if the atrial natriuretic peptide (ANP) is an important factor for inducing diuresis during head-out water immersion even in dehydrated subjects, six healthy volunteers were immersed up to the neck in water at 34.5° C for three hrs. Significant diuresis and natriuresis occurred, but urine osmolality decreased and negative

ATRIAL NATRIURETIC PEPTIDE LEVELS IN TREATED CONGESTIVE HEART FAILURE

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Factors predicting mortality in patients after myocardial infarction caused by left main coronary artery occlusion: significance of ST segment elevation in both aVR and aVL leads.

was restored in a positive direction toward zero, even though subjects were still in a state of considerable dehydration. Plasma renin activity and plasma angiotensin I and II concentrations decreased but that of plasma aldosterone remained unchanged during water immersion, and plasma ANP did not increase thoughout the examination. On the basis of the data of the present study, the factor inducing diuresis during head-out water immersion in hydrated subjects appears to differ from that in dehydrated subjects, and the main factor inducing diuresis during water immersion in dehydrated subjects may be the suppression of vasopressin release and not ANP.