Search PubMed⌕ Search

Biomedical subjects

Y Koiwaya

Publications and source records attributed to Y Koiwaya.

At least 73 records · Page 4Linked to original sources
PubMed1985

Coronary artery spasm immediately after percutaneous transluminal coronary recanalization.

A 55-year-old man developed acute inferior myocardial infarction. A coronary arteriogram performed within two hours later showed complete occlusion of the right coronary artery, which was not resolved by two doses of 300 micrograms of intracoronary nitroglycerin. It was recanalized with 50% luminal diameter narrowing after 600,000 units of urokinase. Immediately after this thrombolytic therapy, the patient experienced chest pain, and the coronary artery became completely obstructed again. The pain was promptly relieved by 300 micrograms of intracoronary nitroglycerin, with disappearance of the obstruction. The observations during the procedure indicate that coronary artery spasm can occur after successful thrombolytic therapy on an occluded artery, inducing postinfarction angina, and might culminate in a second complete occlusion after percutaneous transluminal coronary recanalization.

Angioplasty, Balloon↗
PubMed1985

Cyclic sinus node dysfunction in a patient with hyperthyroidism.

In a 54-year-old woman with hyperthyroidism, episodic sinus node dysfunction (SND) recurred in a cyclic fashion. The SND occurred suddenly during normal sinus rhythm and progressed to marked sinus bradycardia; occasionally, sinus arrest developed with or without ventricular escape beats. A 1-mg dose of intravenous atropine sulfate suppressed the occurrence transiently. After a 200-mg dose of propylthiouracil and a 20-mg dose of prednisolone every six hours, the SND was completely abolished within 21 hours. It is probable that, together with a pathologic process induced by hyperthyroidism, the autonomic nervous system participated in our patient's episodic SND.

Arrhythmias, Cardiac↗
PubMed1984

Clinical characteristics and prognosis of patients with postinfarction angina caused by coronary artery spasm.

Clinical features and the course of 15 patients with postinfarction angina caused by coronary artery spasm are described. Episodes of postinfarction angina in the patients recurred at rest in the early recovery phase and were accompanied by transient ST-segment elevation. The area where ST-segment elevations were demonstrated on a 12-lead ECG always included the leads with newly developed abnormal Q waves. Pain resolved spontaneously or after sublingual nitroglycerin in several minutes. Holter ECGs during a 24-h period demonstrated frequent episodes of ST-segment elevation that were not always associated with chest pain. Treatment with calcium antagonist and/or nitrates effectively suppressed angina, and only one patient developed reinfarction. The patient's subjective symptoms were abolished by diltiazem and isosorbide dinitrate. A Holter ECG of the patient revealed silent ST-segment elevations before and after the reinfarction and an increase of the drugs completely suppressed the recurrence of silent ischemic ECG changes. Coronary arteriograms were obtained from 8 patients, which demonstrated more than 75% segmental stenosis on one coronary artery in 5 patients and no significant obstruction in the remaining 3. All patients performed a treadmill exercise stress test before discharge and most demonstrated excellent tolerance. All patients experienced no form of chest pain for an average of 25 months follow-up under medication. We conclude that among patients with postinfarction angina, those cases caused by coronary artery spasm have a relatively good prognosis.

Adult↗
PubMed1984

Elimination of unstable angina by diltiazem under temporary pacing.

We describe two patients in whom spontaneous angina following acute myocardial infarction (postinfarction angina caused by coronary artery spasm) and worsening angina were successfully eliminated after clinical dosage of oral diltiazem, while marked sinus node suppression developed and temporary pacing was performed. The patients were females (one was 67 years and one was 64 years old), and had no history of sinus node dysfunction. The occurrence of the adverse effect was not during angina, and the intervals between the initiation of diltiazem and the occurrence were 6 days after 120 mg/day in one patient, and 4 h after a single administration of 60 mg in the other. Diltiazem is also efficacious in the elimination of unstable angina, however one should note that diltiazem may remarkably suppress not only atrioventricular node activity but also sinus node activity in some patients.

Aged↗
PubMed1984

Transient U wave inversion during variant angina.

We studied the prevalence and clinical significance of transient U wave inversion in 43 patients with variant angina. Twenty-four patients (group A) had ST segment elevation in the anterolateral and 19 patients (group B) had this finding in the inferoposterior leads of the ECG during spontaneous angina. In none of these patients was U wave inversion present on the resting 12-lead ECG in the absence of anginal attack. During anginal attacks, U wave inversion developed in association with ST segment elevation in 16 patients (66.7%) of group A but in no patient of group B. To exclude the possibility that a transient rise of systolic blood pressure during angina caused U wave inversion, treadmill exercise testing was done in the 16 patients after the discontinuation of antianginal drugs. In 12 of the 16 patients, exercise testing did not produce angina or U wave inversion despite a marked elevation of systolic blood pressure. These results indicate that transient U wave inversion frequently develops with anterolateral ischemia but not with inferoposterior ischemia during attacks of variant angina. It is likely that transient U wave inversion was caused by myocardial ischemia but not by a rise of blood pressure during angina.

Adult↗
PubMed1984

Reflex heart rate and blood pressure changes during ST segment elevation in patients with variant angina.

Responses of heart rate and blood pressure to transient myocardial ischemia were analyzed in patients with variant angina. Heart rate changes during ST segment elevation were examined by means of a Holter ECG monitoring system. All 27 ST segment elevations from 10 patients with anterior ischemia were accompanied by an increase in heart rate by 12 +/- 2 bpm (mean +/- SEM, p less than 0.001) at peak ST segment elevation. With inferior ischemia in nine patients, heart rate decreased significantly by 4 +/- 1 bpm (n = 28, p less than 0.001). However, 9 of these 28 ST segment elevations showed a biphasic response of heart rate, that is, an initial increase and subsequent decrease. Such heart rate changes were not different between ST segment elevations with and without chest pain. With chest pain systolic blood pressure rose in anterior ischemia by 42 +/- 5 mm Hg (n = 10, p less than 0.001) but fell in inferior ischemia by 22 +/- 8 mm Hg (n = 7, p less than 0.05). We conclude that a different cardiovascular reflex occurs in response to inferior versus anterior ischemia and it is independent of chest pain.

Aged↗
PubMed1984

Steroid therapy in cardiac sarcoidosis. Increased left ventricular contractility concomitant with electrocardiographic improvement after prednisolone.

A 23-year-old woman was referred to our clinic because of pulmonary edema. The electrocardiogram on admission demonstrated eventual QS pattern in leads 1 and a VL with a poor progression of the R-wave amplitude in the precordial leads. The left ventricle was remarkably dilated with severely diminished contractility. Biopsy of the inguinal lymph nodes, liver, and myocardium confirmed the diagnosis of generalized sarcoidosis. After administration of prednisolone, the left ventricular dimension decreased, and contractility increased concomitant with an improvement of the electrocardiographic abnormalities without any aneurysm forming. We conclude that steroids may keep some jeopardized myocardium viable and that initiation of steroid therapy in an early phase does not result in formation of an aneurysm.

Adult↗
PubMed1983

Diurnal distribution of ST-segment elevation and related arrhythmias in patients with variant angina: a study by ambulatory ECG monitoring.

Twenty-four-hour ambulatory ECG recording was performed in 26 patients with variant angina to evaluate the diurnal distribution of ST-segment elevation in relation to chest pain and the incidence of arrhythmias during the episodes. During a recording period of 52 days, 364 ST-segment elevations of 1 mm or greater were observed and 79% were asymptomatic. ST-segment elevation frequently occurred between 0:00 and 9:00 hours (72%) and most frequently between 5:00 and 6:00 hours (13%). Only a few episodes occurred between 10:00 and 18:00 hours. Premature atrial contractions, premature ventricular contractions (PVCs), ventricular tachycardia (VT) and complete atrioventricular block occurred during 12% of the episodes and were more common during painful episodes (32%) than during painless ones (6%). However, VT and severe forms of PVCs (couplets and bigeminy) appeared eight times during painless episodes and nine times during painful ones. Arrhythmias occurred more frequently when the elevated ST segment started to return or was returning to the control level (n = 38) than when the ST segment was rising (n = 8). The incidence of arrhythmias was lower when the daily frequency of ischemic episodes was high. This study shows that episodes of asymptomatic coronary artery spasm predominantly occur early in the morning as symptomatic episodes; complex dysrhythmias appear during the asymptomatic episodes; arrhythmias occur predominantly during a "reperfusion period;" and more arrhythmias accompany infrequent daily episodes of ischemia than frequent ones.

Adult↗
PubMed1983

Effect of diltiazem on recurrent spontaneous angina after acute myocardial infarction.

This study examined the effects of diltiazem, a calcium antagonist, on suppressing spontaneous angina following acute myocardial infarction. Twelve patients developed rest angina within a few days after the onset of acute myocardial infarction, which was associated with transient S-T segment elevation. A 24-hour recording of electrocardiogram revealed cyclic S-T segment elevation with or without chest pain in all patients. A selective coronary arteriography was performed in seven patients which demonstrated no critical stenosis, despite acute myocardial infarction, in three patients. In one of these three patients, coronary artery spasm was induced by ergonovine in the vessel supplying the acutely infarcted area. These clinical features suggested that spontaneous angina in these patients probably was caused by spasm of the coronary artery. Diltiazem suppressed rest angina as well as painless cyclic S-T segment elevation completely in all 12 patients. The replacement of diltiazem with placebo in two patients caused the recurrence of rest angina. Thus, we conclude that diltiazem is effective in the treatment of postinfarction angina caused by coronary artery spasm.

Aged↗
PubMed1982

Postinfarction angina caused by coronary arterial spasm.

Recurrent ST-segment elevations in leads where new Q waves developed were repeatedly recorded in six patients during a recovery phase of acute myocardial infarction. Such ST-segment elevations were transient, occurred with or without chest pain, and returned to control levels. No enzymatic changes signifying recurrent myocardial necrosis were found after each episode. Selective coronary cineangiography in one patient demonstrated a mild segmental stenosis in the coronary artery perfusing the infarcted area; this artery became completely occluded after administration of i.v. ergonovine. Administration of calcium antagonists effectively reduced the frequency of postinfarction angina and ST-segment elevations. The clinical features suggest that the postinfarction angina in these patients is produced by coronary arterial spasm and that coronary arterial spasm may cause severe life-threatening dysrhythmias.

Adult↗