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Biomedical subjects

J C Kaski

Publications and source records attributed to J C Kaski.

171 records · Page 10Linked to original sources
PubMed1985

Different susceptibility to myocardial ischemia provoked by hyperventilation and cold pressor test in exertional and variant angina pectoris.

Coronary constriction at the site of atherosclerotic stenoses has been suggested to play an important role in modulating the frequency of symptoms in patients with exertional angina. To investigate whether stimuli triggering coronary constriction have similar effects in patients with exertional and variant angina, responses to hyperventilation (HV) and cold pressor test (CPT) were evaluated. Twenty patients with chronic exertional angina, positive exercise test results and coronary heart disease were compared with 14 patients with variant angina and ST-segment elevation during an ergonovine test. In patients with exertional angina, the CPT produced diagnostic ST-segment depression in 6 of 20 patients (30%) at levels of rate-pressure product much lower than those during the exercise test; all patients had low effort tolerance and severe coronary artery disease. HV produced diagnostic ST-segment depression in only 1 of 20 patients (5%) (p less than 0.05 compared to that with CPT). Conversely, in patients with variant angina, HV produced ST-segment elevation in 11 of 14 patients (78%) and CPT produced elevation in only 2 of 14 (14%) (p less than 0.01). Thus, coronary constriction can provoke myocardial ischemia not only in patients with variant angina but also in some patients with exertional angina. Furthermore, the 2 groups of patients have a different susceptibility to stimuli known to produce coronary constriction.

Adult↗
PubMed1985

Efficacy of carvedilol (BM 14,190), a new beta-blocking drug with vasodilating properties, in exercise-induced ischemia.

The exercise response to a single oral dose (25 mg) of a new beta-blocking agent that also has potent vasodilating properties, carvedilol (BM 14,190), was assessed in 15 patients with stable exertional angina, positive exercise test responses (greater than or equal to 1 mm of ST depression) and coronary artery disease. A single-blind, placebo-controlled, randomized, crossover design was used. Compared with placebo, 25 mg of carvedilol significantly reduced both heart rate (HR) and blood pressure (BP) at rest (p less than 0.01). After administration of carvedilol, 10 of 15 patients did not have angina at peak exercise (p less than 0.01) and 5 had ST shifts of less than 1 mm (p less than 0.05). Total exercise time and time to 1 mm of ST depression were prolonged and ST-segment depression at peak exercise was significantly reduced (p less than 0.01). Systolic BP was reduced both at peak exercise and at 1 mm of ST depression (p less than 0.05), whereas mean HR at peak exercise did not change significantly compared with placebo. Overall, mean HR-BP product at peak exercise was significantly reduced by carvedilol compared with placebo (p less than 0.05). However, 4 patients actually achieved a higher HR-BP product but did not have angina and had less ST depression (or no ST-segment shifts) at peak exercise. This indicates an increase in their coronary flow reserve. These results suggest that carvedilol is effective therapy for effort-induced angina, and this may be related to its combined beta-blocking and potent vasodilatory properties.

Adrenergic beta-Antagonists↗
PubMed1985

Improved coronary supply: prevailing mechanism of action of nitrates in chronic stable angina.

Exercise tolerance before and after sublingual isosorbide dinitrate (ISDN), 10 mg, was assessed in 217 consecutive patients with stable angina, positive exercise test, and angiographically proved coronary artery disease. In 65 patients (30%), ISDN prevented exercise-induced ST segment depression and/or increased exercise time to 1 mm ST segment depression (greater than or equal to 3 minutes), despite the significantly higher (greater than or equal to 25 X 10(2) increment) rate-pressure product attained (increased coronary reserve). On the contrary, in 40 other patients, exercise test remained positive, and neither time to 1 mm ST segment depression nor rate-pressure product increased significantly (fixed coronary reserve). The remaining 106 patients had an intermediate response. To assess the mechanisms underlying the beneficial action of nitrates, we further investigated 13 patients with increased coronary reserve (group 1) and five with fixed coronary reserve (group 2) by the exercise response to ISDN and verapamil, the changes in left ventricular volumes after ISDN and verapamil, the ECG response to intravenous ergonovine, and the changes in coronary stenosis severity following intravenous ergonovine and intracoronary nitrates. ISDN dramatically improved exercise capacity only in group 1 patients. However, it induced a significant reduction of left ventricular volumes in both groups (p less than 0.01). Ergonovine provoked angina and ST segment depression in 62% of group 1 patients and significantly increased the severity of their coronary stenoses (p less than 0.01). In all group 2 patients, ergonovine was negative, and no significant increase in stenosis severity was observed. Intracoronary nitrates reduced stenosis severity in group 1 (p less than 0.01) but not in group 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Efficacy of amiodarone during long-term treatment of potentially dangerous ventricular arrhythmias in patients with chronic stable ischemic heart disease.

Amiodarone was administered orally to 30 patients with chronic stable coronary artery disease and severe ventricular arrhythmias. Control studies revealed frequent (more than 30/hr) ventricular premature beats (VPBs) (27 patients), bigeminy (21 patients), couples (29 patients), R-on-T phenomenon (14 patients), ventricular tachycardia (16 patients), and ventricular fibrillation (1 patient). Two 24-hour Holter recordings and stress tests were performed before treatment, and an average of 3.6 per patient were done during treatment. Amiodarone caused suppression of all ventricular arrhythmias in 13 (43%) of the 30 patients and suppression of all complex forms and greater than 90% reduction of VPB number in 14 patients (47%) during a follow-up of 12.4 months. The mean dose was 590 mg/day in the 27 responders and 300 mg/day in the three nonresponders. A similar antiarrhythmic response was observed during stress testing. One of the 30 patients died due to massive pulmonary embolism and no arrhythmias were detected. In addition, amiodarone suppressed the occurrence of anginal pain and effort-induced ST changes in 9 of 10 patients and in 11 of 13 patients, respectively. The rate-pressure product and peak heart rate were significantly reduced in all patients. Our results suggest that amiodarone may be ideally suited for treatment of ventricular arrhythmias and for possible prevention of sudden death in patients with ischemic heart disease.

Adult↗
PubMed1984

Myocardial ischemia during ergonovine testing: different susceptibility to coronary vasoconstriction in patients with exertional and variant angina.

Coronary spasm is an accepted cause of transient myocardial ischemia in patients with variant angina; more recently it has been suggested that dynamic stenoses could also play an important role in the pathophysiology of exertional angina. To test this hypothesis we submitted 31 patients with histories typical of exertional angina to ergonovine testing and compared the electrocardiographic and clinical responses to those observed in seven patients with variant angina. All underwent bicycle ergometric exercise testing and coronary angiographic examination. For all tests, ST segment shifts of 0.1 mV or greater were considered to be diagnostic of myocardial ischemia. In patients with exertional angina, exercise testing produced diagnostic ST segment depression in 21 (68%). Ergonovine testing produced diagnostic ST segment depression in nine (29%). All nine had positive exercise test results and two- or three-vessel disease, yet the test was negative in seven other patients with positive exercise test results and similar angiographic findings. Conversely, in the seven patients with variant angina, results of exercise testing were positive in five (ST segment depression in two, ST elevation in three), while ergonovine produced ST segment elevation in all seven. Coronary angiographic examination showed normal arteries in two, one-vessel disease in four, and three-vessel disease in one. Results of all ergonovine tests were positive at values of rate pressure product much lower than those observed during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

The hyperventilation test as a method for developing successful therapy in Prinzmetal's angina.

In 10 cases of Prinzmetal's angina in which episodes of myocardial ischemia were easily and reproducibly induced by hyperventilation, this test was performed 111 times, 41 times under control conditions and 70 times during treatment with one or more of the following drugs: phentolamine, isosorbide dinitrate, propranolol, verapamil, nifedipine and amiodarone. Seventeen of 18 negative tests performed under the influence of a long-acting drug coincided with total remission of the patient's anginal episodes when this drug was administered on a short- or long-term basis. No patient died or sustained infarction during a follow-up period of 10.9 months. A negative test was thus a good indication that the clinical response to the corresponding drug would be favorable. The electrocardiographic changes and chest pain provoked by hyperventilation occurred not when alkalosis was greatest (hydrogen ion [pH] change from 7.42 to 7.58, p less than 0.001), but when pH was approaching normal or control values. The onset of electrocardiographic changes occurred an average of 175 seconds after the end of hyperventilation and, in two cases, the time lag was as much as 480 and 705 seconds, respectively. This raises several questions regarding the true mechanism triggering coronary spasm under such conditions. The hyperventilation test appears to be a useful and safe procedure for selecting the best possible drug for long-term treatment of Prinzmetal's angina as well as for comparing the relative efficacy of different drugs.

Adult↗
PubMed1981

Long-term management of sustained, recurrent, symptomatic ventricular tachycardia with amiodarone.

Twenty-three patients with sustained, recurrent, symptomatic ventricular tachycardia were treated with oral amiodarone. Initial doses were 600-2000 mg/day and maintenance doses were 200-1200 mg/day. Amiodarone was highly effective in 20 patients (87%), seven of whom had a follow-up of 30 months or longer, including two who were followed for 5 years. Three patients died within the first 45 days, three died suddenly after a follow-up of 33.5 months, and four had a nonarrhythmic death after a follow-up of 25 months. Fifteen patients (65%) had no recurrence during a follow-up of 21.5 months, while five (22%) had isolated recurrences during a follow-up of 32.2 months. The average maintenance dose was 713 mg/day in the 15 patients who did not have recurrences and 375 mg/day in the five patients who had recurrences (p less than 0.001). Both short- and long-term tolerance were excellent and there was not a single case in which treatment had to be discontinued. The main disadvantage of amiodarone was that it took an average of 9.5 days to reach anti-arrhythmic efficacy. The main advantages were prolonged duration of action (recurrences occurred only 15-60 days after the drug was discontinued or the dose lowered, virtual absence of contraindications, doses as high as 2000 mg/day were safe and patient compliance was excellent.

Adult↗