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Biomedical subjects

J C Kaski

Publications and source records attributed to J C Kaski.

At least 163 records · Page 9Linked to original sources
PubMed1989

Effects of diltiazem alone or with isosorbide dinitrate or with atenolol both acutely and chronically for stable angina pectoris.

To establish the contribution of combination therapy in stable angina, the short- and long-term effects of diltiazem (120 mg and 360 mg/day, respectively), and the additive effects of sublingual isosorbide dinitrate, 10 mg, and atenolol, 100 mg, were studied in 11 patients with chronic stable angina using an open-label sequential design. All patients underwent exercise testing without therapy, and with each drug and their combinations. Exercise time and heart rate-blood pressure product were measured at 1-mm ST-segment depression, or at peak exercise if the test result was negative. Exercise time increased from a control value of 8.0 +/- 2.3 minutes (mean +/- standard deviation) to 11.4 +/- 2.4 minutes (p less than 0.0001) after the administration of isosorbide dinitrate, to 11.3 +/- 1.8 minutes (p less than 0.001) after short-term diltiazem and to 12.4 +/- 1.5 minutes (p less than 0.001) after long-term diltiazem. The rate-pressure product increased from a control value of 19,070 +/- 3,564 to 24,431 +/- 4,795 beats/min X mm Hg (p less than 0.0001) after isosorbide dinitrate, to 22,287 +/- 4,753 beats/min X mm Hg (p less than 0.01) after short-term diltiazem and to 21,812 +/- 3,976 beats/min X mm Hg (p less than 0.007) after long-term diltiazem. The addition of atenolol to long-term diltiazem significantly reduced the rate-pressure product compared with long-term diltiazem alone (21,812 +/- 3,976 vs 13,926 +/- 2,880 beats/min X mm Hg, (p less than 0.002), although there was no further significant increase in exercise time (12.4 +/- 1.5 vs 13.3 +/- 1.6 minutes).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Lack of evidence for alpha-adrenergic receptor-mediated mechanisms in the genesis of ischemia in syndrome X.

Patients with syndrome X (typical angina pectoris, positive exercise tests [greater than or equal to 1 mm of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries) have a reduced coronary flow reserve due to inappropriate dilatation of small resistive vessels. To assess whether alpha-adrenergic mechanisms play a role in the genesis of ST-ischemic changes in syndrome X, 12 patients with this syndrome (2 men and 10 women, mean age 50 +/- 6 years) underwent exercise testing and 24-hour ambulatory electrocardiographic monitoring. They were done off treatment and after alpha blockade with prazosin and clonidine on 2 separate weeks. Despite treatment, all exercise tests remained positive and patients were stopped because of progressive angina pain. Compared to the off-treatment tests, exercise duration and heart rate-blood pressure product at 1 mm of ST-segment depression did not change significantly after prazosin (617 +/- 203 vs 663 +/- 203 seconds and 23,857 +/- 6,125 vs 22,098 +/- 4,816 beats/min X mm Hg, respectively) and clonidine (684 +/- 148 vs 649 +/- 80 seconds and 25,514 +/- 2,386 vs 24,567 +/- 2,001 beats/min X mm Hg, respectively). Ambulatory monitoring showed similar results regarding number of episodes of ST-segment depression greater than or equal to 0.1 mV during control and after prazosin (39 vs 38) or clonidine (26 vs 23) treatment. None of the 8 patients who also underwent provocative testing with phenylephrine had ischemic electrocardiographic changes; only 2 experienced chest pain during the test.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Long-term variability of angina pectoris and electrocardiographic signs of ischemia in syndrome X.

The long-term course of angina and the electrocardiographic signs of ischemia were assessed in 13 patients (10 women and 3 men, mean age 49 +/- 6 years) with typical angina pectoris, positive exercise tests, no evidence of coronary spasm and angiographically normal coronary arteries (syndrome X). Clinical and electrocardiographic parameters as well as results of exercise testing and 24-hour electrocardiographic monitoring were assessed at presentation and after a mean follow-up of 6.3 years (range 3 to 9). Mean number of anginal episodes and nitroglycerin consumption per week were similar at presentation and at the last follow-up. Furthermore, no significant difference was noted in heart rate-systolic blood pressure product at 0.1 mV of ST-segment depression (20,363 +/- 5,747 vs 21,649 +/- 5,687 beats/min x mm Hg), at angina (19,223 +/- 5,680 vs 20,126 +/- 6,023 beats/min x mm Hg) and at peak exercise (22,057 +/- 5,669 vs 22,868 +/- 6,122 beats/min x mm Hg). Time to 0.1 mV of ST-segment depression, to angina and to peak exercise was also similar (595 +/- 163 vs 631 +/- 184 s, 524 +/- 156 vs 571 +/- 168 s and 671 +/- 168 vs 718 +/- 186 s, respectively). The number of episodes of ST-segment depression greater than or equal to 0.1 mV during electrocardiographic monitoring was similar at presentation and follow-up (31 vs 25) as was the proportion of painful episodes (39 vs 36%). None of the patients developed major coronary events or cardiomyopathy during follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Effect of theophylline on exercise-induced myocardial ischaemia.

In a single-blind, placebo-controlled, randomised trial in 20 patients with stable angina pectoris, intravenous theophylline ethylenediamine (aminophylline), 7 mg/kg, increased the time to onset of angina by 46%, the heart-rate/blood-pressure product (an index of myocardial oxygen consumption) at 1 mm ST segment depression by 22%, and exercise duration by 24%. In a subsequent double-blind placebo-controlled trial in 8 patients a single oral dose of theophylline (375 mg) increased the time to onset of angina by 56%, the heart-rate/blood-pressure product at 1 mm ST segment depression by 22%, and the exercise duration by 35%. Infusion of theophylline ethylenediamine during angiography (10 patients) did not affect the diameter of epicardial coronary arteries. The beneficial effects of theophylline may be due to redistribution of coronary blood flow from non-ischaemic to ischaemic myocardium.

Administration, Oral↗
PubMed1989

Ischemic threshold varies in response to different types of exercise in patients with chronic stable angina.

The effects of different types of exercise on ischemic threshold were studied in 33 patients with chronic stable angina, documented coronary artery disease, and reproducible positive exercise test results. On average, ST segment depression developed at a significantly higher heart rate and rate-pressure product when the standard modified Bruce protocol was preceded by a warm-up period (113 +/- 13 vs 119 +/- 15 beats/min and 18,813 +/- 3682 vs 20,357 +/- 4227 beats/min X mm Hg, respectively; p less than 0.05 and less than 0.01). No significant changes were observed when the exercise was started abruptly. Analysis of results in individual patients showed that changes in rate-pressure product at 1 mm ST segment depression greater than or equal to 2000 beats/min X mm Hg developed with different types of exercise in 11 patients (group I), whereas in 22 patients little or no change occurred (group II). All patients also underwent exercise testing before and after 0.5 mg of sublingual nitroglycerin; improvement induced by nitroglycerin was significantly greater in group I than in group II (22 +/- 8 vs 8 +/- 9 beats/min and 4896 +/- 1998 vs 1064 +/- 2145 beats/min X mm Hg; p less than 0.01). Furthermore, isometric handgrip exercise carried out during angiography resulted in significant reduction of luminal diameter at the site of the stenosis of group I (1.22 +/- 0.39 vs 0.99 +/- 0.35 mm; p less than 0.01) but not in group II (1.12 +/- 0.22 vs 1.16 +/- 0.3 mm, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Adenosine-induced chest pain in patients with silent and painful myocardial ischaemia: another clue to the importance of generalized defective perception of painful stimuli as a cause of silent ischaemia.

Adenosine is formed from adenosine triphosphate within the ischaemic cells from where it is released into the coronary circulation. Adenosine exhibits several cardiovascular effects which tend to protect the ischaemic myocardium. Based on the observation that in healthy volunteers the intravenous infusion of adenosine produces angina-like chest pain, it has been recently proposed that another cardioprotective action of this substance could be provocation of angina. If this is the case adenosine should not produce chest pain in patients with silent ischaemia. To test this hypothesis we infused this substance intravenously at increasing doses of 50, 100, 150, 200, 250 and 300 micrograms kg-1 min-1 in eight patients with silent ischaemia (group A). All of them developed ST depression (1.8 +/- 0.2 mm) during exercise testing and seven also during adenosine infusion (1.1 +/- 0.8 mm). However, none of the patients had chest pain during exercise while seven had chest pain during adenosine. We then infused adenosine in eight other patients (Group B) who had painful ischaemia and an exercise tolerance similar to that of Group A patients (time to 1 mm ST depression 8.6 +/- 2.7 min and 8.4 +/- 3 min, respectively, P = NS). Adenosine induced chest pain in all Group B patients. The time to pain onset during adenosine was similar in the two groups (9.3 +/- 2.3 min in Group B and 12.4 +/- 4.9 min in Group A).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1987

Pain threshold and tolerance in women with syndrome X and women with stable angina pectoris.

A recent report showed that during Holter monitoring of patients with syndrome X (typical anginal pain, positive exercise test response [at least 0.1 mV of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries), 50% of episodes of ischemic ST-segment depression were painful. This proportion is considerably higher than that in patients with chronic stable angina, which is about 30%. A significantly lower threshold and tolerance to painful stimuli was seen in a group of patients with chronic stable angina in whom 50% of episodes were painful compared with a group in whom only 5% of episodes were silent. Hence, patients with syndrome X may have enhanced sensitivity to painful stimuli. To investigate whether this difference was due to a lower threshold for painful stimuli in general, 12 patients with syndrome X and 10 (age- and sex-matched) with chronic stable angina were studied using the same battery of painful stimuli. Patients with syndrome X had a significantly lower threshold and tolerance for forearm ischemia (-36%, p less than 0.05, and -40%, p less than 0.001) and electrical skin stimulation (-37%, p less than 0.01, and -35%, p less than 0.001); the cold pressor test did not show significant differences (-7%, p = 0.391, and -1%, p = 0.818). Thus, patients with syndrome X in this study had significantly lower threshold and tolerance values for forearm ischemia and for electrical skin stimulation. These differences in sensitivity to pain may partly explain a higher incidence of painful ischemic episodes detected by ambulatory electrocardiographic monitoring during unrestricted daily life.

Angina Pectoris↗
PubMed1987

Usefulness of Holter monitoring to improve the sensitivity of exercise testing in determining the degree of myocardial revascularization after coronary artery bypass grafting for stable angina pectoris.

To assess whether Holter monitoring improves the sensitivity of exercise testing in identifying incomplete myocardial revascularization, both tests were performed in 45 patients from 3 to 5 months after elective coronary artery bypass grafting (CABG) for stable angina pectoris. Coronary angiography revealed incomplete revascularization in 26 patients. Six of these 26 had 52 episodes of ST-segment depression during Holter monitoring and myocardial ischemia during exercise testing. Their exercise capacity was significantly lower than that of 10 other patients in whom the results of exercise testing only were positive (heart rate at 0.1 mV ST-segment depression 112 +/- 9 vs 123 +/- 15 beats/min, p less than 0.001). In the other 10 patients with incomplete myocardial revascularization the results of both investigations were negative. The graft patency rate was lower in patients with a positive response to exercise testing than in those with a negative response (52% vs 71%, p less than 0.005). Myocardial revascularization was angiographically complete in 19 patients. In 18 of these 19 patients the findings of both investigations were negative; in 1 patient Holter monitoring revealed episodes of ST-segment elevation suggestive of variant angina. Thus, after CABG for stable angina pectoris the results of Holter monitoring do not improve the sensitivity of exercise testing in identifying patients with angiographically incomplete myocardial revascularization because findings are positive only in patients with low exercise capacity. Both tests fail to show evidence of myocardial ischemia in most patients with angiographically complete myocardial revascularization.

Aged↗
PubMed1987

Induction of coronary artery spasm by a direct local action of ergonovine.

To investigate whether ergonovine acts directly on coronary arteries or via remote neurohumoral reflexes, we administered small titrated increments of intracoronary ergonovine up to a maximum cumulative dose of 50 micrograms to 15 patients. In six patients with variant angina (group 1), ischemic electrocardiographic ST changes, angina, and localized coronary spasm (local coronary diameter reduction of 87.8 +/- 18.9% [mean +/- SD]) followed after 6 to 50 micrograms (mean 20.7) cumulative intracoronary ergonovine. In nine patients with atypical chest pain, normal baseline coronary arteriograms, and no evidence of variant angina (group 2), there was no ischemic ST segment change or localized coronary spasm after 6 to 50 micrograms (mean 31.6) intracoronary ergonovine. Coronary diameter of proximal vessels of patients in group 2 was reduced by 16.2 +/- 6.5% and did not differ from the response of nonspastic vessels of comparable size of group 1 (20.5 +/- 13.8%; p = .7). There was no significant difference in the median effective dose values in the dose-response curves of the spastic and nonspastic segments between groups 1 and 2. Ergonovine causes coronary spasm by a direct local effect, which seems to be caused by localized arterial hyperreactivity rather than supersensitivity. Intracoronary delivery may be safer than intravenous administration because negligible drug recirculation may prevent perpetuation of spasm and selective coronary administration can avoid branches with critical stenoses.

Coronary Vasospasm↗
PubMed1987

Efficacy of carvedilol in exercise-induced myocardial ischemia.

The exercise response to a single oral dose (25 mg) of a new beta-blocking agent that also has potent vasodilating properties, carvedilol, was assessed in 15 patients with stable exertional angina, positive exercise tests (greater than or equal to 1 mm ST depression) and coronary artery disease. A placebo-controlled, randomized, crossover study was carried out. Compared with placebo, carvedilol significantly reduced both resting heart rate (HR) and blood pressure (BP) at rest. After the administration of carvedilol, 10 of the 15 patients did not have angina at peak exercise and 5 had ST shifts less than 1 mm. Total exercise time and time to 1 mm ST depression were prolonged, and ST segment depression at peak exercise was significantly reduced. Systolic BP was reduced both at peak exercise and at 1 mm ST depression 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. However, four patients achieved similar or higher HR-BP product and yet did not experience angina and had less ST depression (or no ST segment shifts) during 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 vasodilatory properties.

Adrenergic beta-Antagonists↗
PubMed1986

Transient myocardial ischemia during daily life in patients with syndrome X.

Nineteen patients with syndrome X (typical exertional angina, positive exercise test response [at least 0.1 mV of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries) underwent continuous 48-hour electrocardiographic (ECG) monitoring during unrestricted daily life. Fifty-eight ischemic episodes of at least 0.1 mV of ST-segment depression were observed in the same ECG leads that showed ST depression during stress testing: 28 (48%) were accompanied by anginal pain and 30 (52%) were asymptomatic. No significant differences were found between painful and silent ST-segment depression with regard to the number of episodes, their temporal distribution, magnitude, duration or heart rate (HR) at onset of ST-segment depression. In the minute preceding ischemic ST shifts, HR did not change in 33% of episodes or increased by less than 10 beats/min in 28%. HR at onset of ST depression was significantly lower during ambulatory ECG monitoring than during exercise testing (98 +/- 18 vs 117 +/- 18 beats/min, p less than 0.01). During ambulatory monitoring, 85 episodes of sinus tachycardia (exceeding by 10 to 80 beats/min the HR that triggered ischemia during exercise testing) occurred in the absence of angina or ST-segment shifts. The results of this study suggest that in patients with syndrome X, myocardial ischemia frequently develops during daily life; silent ischemia is an important component of this syndrome; and increased oxygen demand in the presence of impaired coronary vasodilatory capacity is not the only cause of myocardial ischemia. Active mechanisms that transiently reduce coronary flow may act and explain occurrence of angina at rest and with minimal exertion.

Adult↗
PubMed1986

Variability of results during repeat exercise stress testing in patients with stable angina pectoris: role of dynamic coronary flow reserve.

In some patients with stable angina, the variability of results during repeated exercise tests is higher than in others with similar symptoms. The aim of the study was to assess whether this difference can be explained by a different susceptibility of the coronary arteries to vasoconstrictor stimuli. Ten patients (group A) with stable angina, who developed myocardial ischemia (angina and ST segment depression greater than 0.1 mV) following ergonovine-induced coronary constriction, and 10 other patients (group B) with stable angina, but a negative ergonovine test result, were subjected to two treadmill exercise tests. The variability of heart rate and heart rate-blood pressure product at 0.1 mV ST segment depression was significantly higher in group A than in group B (12 +/- 4 vs 4 +/- 4 bpm, respectively, p less than 0.001 and 3366 +/- 1900 vs 930 +/- 960 bpm X mm Hg, respectively, p less than 0.005), such as the variability of heart rate-blood pressure product at the onset of angina (3887 +/- 2400 vs 1428 +/- 1800 bpm X mm Hg, respectively, p less than 0.04). The remaining exercise parameters were always more variable in group A than in group B, but these differences did not achieve statistical significance. Thus patients with stable angina who develop myocardial ischemia in response to ergonovine have a larger variability of results during repeat exercise testing. Such findings could be explained by an enhanced susceptibility to the coronary constrictor effects of exercise resulting in dynamic changes in coronary flow reserve.

Aged↗
PubMed1986

Increased uptake of 18F-fluorodeoxyglucose in postischemic myocardium of patients with exercise-induced angina.

Regional myocardial perfusion and exogenous glucose uptake were assessed with rubidium-82 (82Rb) and 18F-2-fluoro-2-deoxyglucose (FDG) in 10 normal volunteers and 12 patients with coronary artery disease and stable angina pectoris by means of positron emission tomography. In patients at rest, the myocardial uptake of 82Rb and FDG did not differ significantly from that measured in normal subjects. The exercise test performed within the positron camera in eight patients produced typical chest pain and ischemic electrocardiographic changes in all. In each of the eight patients a region of reduced cation uptake was demonstrated in the 82Rb scan recorded at peak exercise, after which uptake of 82Rb returned to the control value 5 to 14 min after the end of the exercise. In these patients, FDG was injected in the recovery phase when all the variables that were altered during exercise, including regional myocardial 82Rb uptake, had returned to control values. In all but one patient, FDG accumulation in the regions of reduced 82Rb uptake during exercise was significantly higher than that in the nonischemic regions, i.e., the ones with a normal increment of 82Rb uptake on exercise. In the nonischemic areas, FDG uptake was not significantly different from that found in normal subjects after exercise. In conclusion, myocardial glucose transport and phosphorylation seem to be enhanced in the postischemic myocardium of patients with exercise-induced ischemia.

Adult↗
PubMed1986

Provocation of coronary spasm by dopamine in patients with active variant angina pectoris.

The effects of dopamine on arteries are different depending on the dose, route of administration, and receptor population. Its administration can cause vasodilation by stimulation of dopaminergic receptors, vasoconstriction by stimulation of alpha-adrenergic and serotonergic receptors, and even spasm of cerebral arteries when given intracisternally in dogs. The ability of dopamine to provoke coronary spasm was assessed in 18 patients with active vasospastic angina in whom this amine was infused at rates of 5, 10, and 15 micrograms/kg/min for periods of 5 min each. The 12-lead electrocardiogram and blood pressure (cuff) were monitored throughout the whole test. In nine patients dopamine caused angina and ischemic electrocardiographic changes suggestive of coronary spasm: ST segment elevation in six patients and ST segment depression in the absence of important coronary stenoses in the remaining three. Infusion of dopamine was repeated during coronary angiography in three patients with positive test results: this provoked occlusive coronary spasm with ST segment elevation in two patients and nonocclusive spasm with ST segment depression in the remainder. In conclusion, infusion of dopamine provokes coronary spasm in a sizeable proportion of patients with active vasospastic angina. Its administration may be detrimental in patients susceptible to coronary spasm, such as those with acute myocardial infarction.

Adult↗
PubMed1986

Local coronary supersensitivity to diverse vasoconstrictive stimuli in patients with variant angina.

It has been shown in different groups of patients with variant angina that coronary spasm can be reproduced by physiologic maneuvers and pharmacologic agents. It is not known, however, to what extent different stimuli can induce spasm in the same patient. To investigate whether coronary arterial spasm results from specific abnormal agonist-receptor interactions or from a local nonspecific coronary supersensitivity to different stimuli, 28 patients with vasospastic angina were submitted to a series of diverse vasoconstrictive stimuli known to provoke coronary spasm. Ergonovine, hyperventilation, handgrip, cold pressor, and exercise-tests, were carried out in all 28 patients. In the last 15 patients histamine was also administered. Spasm was provoked by ergonovine in 96% of patients, by hyperventilation in 54%, by histamine in 47%, by exercise in 46%, and by the cold pressor and handgrip tests in 11% and 7%, respectively. No significant differences were found in the responses to provocative tests of patients with normal coronary arteries or nonsignificant stenoses and those with significant lesions. In the same individual, spasm was induced by at least two vasoconstrictive stimuli, although with a different mechanism of action, in 82% of patients and spasm was induced by three or more stimuli in 39%. Tests were repeated in at least 23 patients and short-term reproducibility paralleled sensitivity. These results suggest that in patients with variant angina, a local nonspecific supersensitivity rather than an abnormal specific agonist-receptor interaction plays a major role in the genesis of coronary arterial spasm.

Adult↗
PubMed1985

Mixed angina pectoris.

Patients who present with episodes of angina caused both by an increase in oxygen demand and by transient impairment of supply have a mixed form of angina. Distinctive clinical features allow the classification of patients in everyday practice. At one end of the spectrum are patients who have angina only and always when they exercise beyond an essentially fixed level; their angina is fairly predictable and has been termed secondary angina. At the other end of the spectrum are patients who have a normal exercise tolerance but have angina at rest or during activities usually well tolerated that must be caused by a transient impairment of coronary blood flow; their angina is typically unpredictable and has been termed primary angina. We adopted the term primary to emphasize the possible existence of multiple causes of impairment of coronary flow, which together are to be contrasted with the traditional prevailing concept of angina being secondary to excessive increase in demand. In between these ends of the spectrum are most of the patients with angina pectoris encountered in clinical practice: they have a rather predictable ceiling of exercise that they cannot exceed without developing angina, but they also have a variable proportion of unpredictable anginal attacks that occur spontaneously or at levels of activity that are usually well tolerated. We introduced the concept of mixed forms of angina when we became aware that the same patient could experience angina both as a result of an excessive increase in myocardial demand, i.e., secondary angina, and as a result of the transient impairment of coronary blood flow supply, i.e., primary angina.

Angina Pectoris↗