Kokyu to junkan. Respiration & circulation最新文献

To answer questions where and how cardiac hypertrophy occurs, secondary to hypertension and in what state the underlying hemodynamics in the heart is when it develops, various cardiac parameters were measured in 132 patients with hypertension, including cardiothoracic ratio (CTR) as calculated on a posteroanterior view and interval (Y) between the inferior vena cava and posterior outline of the heart 2 cm above their cross section on a lateral view of chest X-ray films, Wezler's parameters of vascular dynamics, Blumberger's systolic time intervals and thickness of the interventricular septum and posterior wall as measured by cardioechography. The patients were divided into two groups by age, the young adult group including 62 ranging from 16 to 35 and the middle age group including 70 from 36 to 60. Association among these parameters were investigated by group. The results are as follows. 1. In the juvenile group, cardiac output was usually increased, and CTR was well correlated with septal thickness. In particular systolic pressure was significantly higher in patients with CTR of 50% or greater than in those with CTR less than 50%. As CTR increased, pre-ejection period (PEP) was prolonged, ejection time (ET)/PEP ratio decreased, stroke volume (Vs) and cardiac output (CO) tended to decrease, and peripheral vascular resistance (W) tended to increase. 2. In the middle-age group, Y was closely associated with thickness of the posterior wall. When the patients were divided into two groups by Y, diastolic pressure in patients having Y of 1.8 cm or greater was significantly higher than that in the rest.(ABSTRACT TRUNCATED AT 250 WORDS)

A case is presented of unruptured aneurysm of the non coronary sinus of Valsalva, causing involvement of A-V node and right coronary artery compression. The patient was a 68 year-old woman with a complaint of general fatigue. Electrocardiogram showed complete A-V block. Computed tomography showed an aneurysm of the non coronary sinus of Valsalva. A temporary pacemaker was implanted, but the patient developed respiratory failure and heart failure and died. At autopsy, macroscopically disseminated tuberculosis was noted in both lungs and kidneys. Microscopically a tuberculous inflammatory lesion extending into the A-V node was found. We report this rare case with some consideration of the literature.

A 53-year-old woman was admitted to the hospital for chest pain with headache, nausea and vomiting, two and a half hours after an intramuscular injection of 6 x 10(6) units of IFN (interferon) alpha 2a, in the 11th week of IFN treatment for chronic hepatitis C. The electrocardiogram (ECG) showed ST depression and T inversion in leads II, III, aVF and V3-V6, as commonly seen in myocardial ischemia. However, emergency coronary angiography (CAG) did not show stenosis or spasms clearly, serum CPK was always within the normal limits, Tc-99m PYP scintigraphy and T1-201 scintigraphy did not show any abnormal uptake or defect, and the echocardiogram did not show any abnormality. She recovered from chest pain and the ischemia-like changes seen on the ECG, after IFN treatment was stopped, and she rested for 7 days from this treatment and other treatment using nitrites and a calcium-antagonist. After recovery, the ECG during exercise and hyperventilation showed changes similar to those seen on admission. From these findings, this case was considered to be precipitated by spasms of coronary microvessels, which were not noticeable in CAG. The cause was thought to be complicated by IFN treatment, because this episode appeared after IFN injection, and improved after stopping IFN treatment.

To contribute for making early diagnosis and treatment of acute pulmonary embolism (APE), we investigated on clinical pictures of 225 patients with APE. Common underlying factors were heart disease, prolonged bed rest, post-surgical state, thrombophlebitis, malignant tumor and post-catheterization state in this order. Dyspnea, chest pain, tachycardia and shock were frequently seen as initial symptoms and signs. Blood screening showed leukocytosis, hypoxemia, hypocapnia and elevated serum LDH. Electrocardiographic findings highly demonstrated were ST.T abnormalities, such as T inversion with ST elevation in V1-3, ST depression in V4-6 and sinus tachycardia. Chest X-rays showed diminished pulmonary vascular marking and pulmonary artery dilation. Right ventricular dilatation were frequently seen on 2-dimensional echocardiograms. Pulmonary artery pressure were elevated up to 49/20 (30) mmHg. Twenty-five percent of the patients died, and the recurrence was seen in 4%. Thus, as soon as APE is suspected by above clinical findings, definitive diagnosis should be obtained by the lung perfusion scan and pulmonary arteriography, then oxygen and thrombolytic agents should be given immediately to prevent the fatal outcome.

Basic fibroblast growth factor (bFGF) is a mitogen that is thought to play a important role in myocyte growth. In previous work, we found the increase of immunoreactivity of bFGF in cardiac myocyte of young SHR and pressure over loaded rat heart, and it suggested that endogenous bFGF which contained high molecular form of bFGF contributes to myocardial hypertrophy. To examine this hypothesis, rhabdomyosarcoma (A 204 cells) derived bFGF was used as wild type bFGF. Extracted bFGF from A 204 cells and nonserum conditioned medium of A 204 cells included high molecular form (22, 24 kd), as well as low molecular (18 kd) bFGF by western blotting, and showed hypertrophic effect in cultured myocardial cells. The hypertrophic effects were indicated in remarkable enlargement of cell size and significant increase in phenylalanine incorporation (x 2.2). The maximum expression of c-myc mRNA by A 204 conditioned medium was observed 30 min after stimulation, and it was also accompanied by an increase of accumulation of alpha skeletal actin mRNA by primer extension. After absorption of heparin binding growth factor from A 204 conditioned medium, it indicated no hypertrophic effects. In conclusion, it is likely that wild type bFGF including high molecular weight form plays a important role in cardiac myocyte growth and hypertrophy.