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Biomedical subjects

J C Kaski

Publications and source records attributed to J C Kaski.

At least 127 records · Page 7Linked to original sources
PubMed1994

Abnormal autonomic control of the cardiovascular system in syndrome X.

Anomalies of autonomic control of the coronary circulation may play a role in the development of syndrome X (angina pectoris, ischemic-appearing results on exercise test, and normal coronary arteriograms). Twenty-six patients with syndrome X and 20 healthy sex- and age-matched control subjects were studied by means of analysis of heart rate variability during 24-hour Holter monitoring. Spectral and nonspectral parameters of heart rate variability were investigated. Mean heart rate was similar in patients with syndrome X and in control subjects. Patients with syndrome X had significantly lower standard deviation of all normal RR intervals, a lower percentage of adjacent normal RR intervals > 50 ms in difference (126.4 +/- 22 vs 149 +/- 43 ms, p < 0.05; 6.3 +/- 4 vs 11.2 +/- 7%, p < 0.05; respectively), and a trend toward lower values of time-domain parameters. Lower values of total power and low frequency were also observed in patients with syndrome X (1273 +/- 693 vs 1790 +/- 989 ms2, p < 0.05; 406 +/- 176 vs 729 +/- 455 ms2, p < 0.01, respectively). An inverse correlation between heart rate and measures of heart rate variability was found in syndrome X but not in control subjects. High- and low-frequency power showed a similar circadian pattern in syndrome X patients and control subjects. Patients and control subjects were then allocated into 2 groups according to the median RR duration: syndrome X1 and control 1 with high mean heart rate, and syndrome X2 and control 2 with low mean heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Effects of angiotensin-converting enzyme inhibition on exercise-induced angina and ST segment depression in patients with microvascular angina.

OBJECTIVES: This study was conducted to test the hypothesis that angiotensin-converting enzyme inhibition may lessen myocardial ischemia in patients with microvascular angina. BACKGROUND: Patients with syndrome X (angina pectoris, positive findings on exercise testing and normal coronary arteriogram) have a reduced coronary vasodilator reserve ("microvascular angina") and may show an increased sympathetic drive. Angiotensin-converting enzyme inhibition attenuates sympathetic coronary vasoconstriction in patients with coronary artery disease. METHODS: Ten patients (seven women and three men, mean age [+/- SD] 53 +/- 6 years) with syndrome X and a reduced coronary flow reserve underwent a randomized, single-blind, crossover, placebo-controlled study of the effects of the angiotensin-converting enzyme inhibitor enalapril on angina and exercise-induced ST segment depression. Assessment was by symptom-limited treadmill exercise testing after 2 weeks of treatment with 10 mg/day of enalapril and after 2 weeks of placebo administration. RESULTS: All patients had positive findings on exercise testing (> or = 1 mm ST segment depression and angina) while taking placebo, whereas six patients had a positive test result (four with angina) during enalapril therapy. Total exercise duration and time to 1 mm of ST segment depression were prolonged by enalapril over those obtained with placebo (mean 779 +/- 141 vs. 690 +/- 148 s, p = 0.006 and 690 +/- 204 vs. 485 +/- 241 s, p = 0.007, respectively). The magnitude of ST segment depression was also less with enalapril than with placebo (mean 1.1 +/- 0.4 vs. 1.5 +/- 0.2 mm, p = 0.004). Heart rate and blood pressure at peak exercise and at 1 mm of ST depression were not significantly different during placebo and enalapril treatment. CONCLUSIONS: Angiotensin-converting enzyme inhibition lessens exercise-induced ischemia in patients with syndrome X and microvascular angina, probably by a direct modulation of coronary microvascular tone, which results in an increased myocardial oxygen supply.

Coronary Circulation↗
PubMed1994

Effects of aminophylline on cardiac function and regional myocardial perfusion: implications regarding its antiischemic action.

Aminophylline improves exercise capacity in patients with angina. Because this drug does not dilate epicardial coronary vessels, its beneficial effect is from either a reduction of myocardial oxygen consumption or an improvement of myocardial blood flow distribution. This study was performed to assess the effects of aminophylline on cardiac function and on regional myocardial perfusion to establish the mechanisms of its antiischemic action. In 10 patients during cardiac catheterization hemodynamic parameters and cardiac volumes were obtained during baseline and after intravenous infusion of aminophylline. Aminophylline decreased left ventricular end-diastolic pressure (from 11 +/- 4 to 4 +/- 2 mmHg, p < 0.001), mean right atrial pressure (from 5 +/- 2 to 2 +/- 1 mmHg, p < 0.01), and left ventricular end-diastolic volume (from 117 +/- 36 to 88 +/- 36 ml, p < 0.01); it increased peak dp/dt (from 1931 +/- 329 to 2430 +/- 540 mmHg/sec, p < 0.001) and heart rate (from 69 +/- 9 to 76 +/- 14 beats/min, p < 0.05) and did not modify systolic aortic pressure (138 +/- 14 vs 137 +/- 16 mmHg, p = not significant [NS]). Estimated oxygen consumption during aminophylline (6.7 +/- 1.3 ml/min/gm) was similar to that during baseline (6.7 +/- 1.4 ml/min/gm). In another study in nine anesthetized dogs with a critical stenosis of the left anterior descending artery, myocardial perfusion was assessed by microspheres during control atrial pacing and during atrial pacing after aminophylline; left atrial pressure was kept constant throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminophylline↗
PubMed1994

Coronary vasodilator reserve, pain perception, and sex in patients with syndrome X.

BACKGROUND: It remains unclear whether myocardial ischemia due to coronary microvascular dysfunction is the cause of chest pain in syndrome X (chest pain, ischemic-like stress ECG despite angiographically normal coronary arteries). To assess the function of the coronary microcirculation and its relation to pain perception, we measured myocardial blood flow (MBF) and coronary vasodilator reserve (CVR) in 29 patients with syndrome X and 20 matched normal control subjects. METHODS AND RESULTS: MBF at rest and after intravenous dipyridamole (0.56 mg.kg-1 over 4 minutes) was measured using positron emission tomography with H2(15)O. CVR was calculated as MBFdipyridamole/MBFrest. ECG changes and chest pain after dipyridamole in syndrome X were compared with those in 35 patients with coronary artery disease (CAD). Resting and postdipyridamole MBFs were homogeneous throughout the left ventricle in syndrome X patients and control subjects. MBF was 1.05 (0.25), mean (SD) versus 1.00 (0.22) mL.min-1.g-1 (P = NS) at rest and 2.73 (0.81) versus 3.00 (1.00) mL.min-1.g-1 (P = NS) after dipyridamole in patients and control subjects, respectively. CVRs were 2.66 (0.76) and 3.06 (1.08) (P = NS) and after correction of resting MBF for rate-pressure product were 2.35 (0.83) and 2.34 (0.90) (P = NS) in patients and control subjects, respectively. Female syndrome X patients had higher resting MBF than males, at 1.18 (0.20) versus 0.88 (0.19) mL.min-1.g-1 (P < .001). Chest pain after dipyridamole occurred in syndrome X as frequently as in CAD (21/29 versus 22/35, P = NS). CONCLUSIONS: When patients with syndrome X are compared with control subjects, no differences are found in MBF either at rest or after dipyridamole, despite syndrome X patients experiencing chest pain after dipyridamole to the same extent as patients with CAD. These findings, together with the absence of any relation among MBF, chest pain, and ECG changes under stress, cast further doubt on ischemia as the basis of the chest pain, at least in the majority of syndrome X patients.

Adult↗
PubMed1994

Creatine kinase MB isoforms: sensitive markers of ischemic myocardial damage.

We investigated the use of creatine kinase (CK) MB isoforms as a marker of myocardial cell injury in a preliminary study of 16 patients with chronic stable angina after successful percutaneous transluminal coronary angioplasty (PTCA) and 25 patients after coronary artery bypass grafting (CABG). Three control groups were studied: apparently healthy volunteers (n = 31), patients undergoing thoracotomy (n = 10), and patients undergoing routine coronary angiography (n = 9). Patients in the PTCA group showed an association between ischemic ST segment changes lasting > 3 min and a transient increase in the MB2/MB1 ratio; however, all had total CK-MB activity within normal limits. Routine coronary angiography subjects had no significant change in MB2/MB1. In the CABG patients, MB2/MB1 peaked within 1 h after the cross-clamp release and returned to baseline by 24 h postoperatively. The median time to peak MM3/MM1 and total CK-MB activity was 2 and 8 h after reperfusion, respectively, returning to baseline values by 2 and 5 days, respectively. After thoracotomy, MB2/MB1 was increased only in elderly patients (n = 5) with risk factors for ischemic heart disease; total CK-MB activity was increased in only three of these. Apparently, CK-MB isoforms can detect myocardial damage in clinical settings with less overt damage than myocardial infarction.

Adolescent↗
PubMed1993

Comparison of regional myocardial blood flow in syndrome X and one-vessel coronary artery disease.

Myocardial blood flow (MBF) was measured using continuous inhalation of oxygen-15-labeled carbon dioxide, and positron emission tomography before and after intravenous dipyridamole in 13 patients with syndrome X (angina pectoris, angiographically normal coronary arteries, positive exercise test and negative ergonovine test), 7 healthy subjects and 8 patients with 1-vessel coronary artery disease (CAD). In patients with syndrome X, baseline MBF was greater than in healthy subjects and patients with CAD (1.24 +/- 0.27 vs 0.87 +/- 0.07 and 1.03 +/- 0.23 ml/g/min, respectively; p < 0.05), and more heterogeneous (34 +/- 7 vs 26 +/- 5 and 25 +/- 6, respectively; p < 0.05) as assessed by the coefficient of variation among myocardial regions < or = 2.3 cm3. After dipyridamole, MBF in patients with syndrome X was similar to that in healthy subjects (2.95 +/- 0.75 vs 3.40 +/- 0.82 ml/g/min; p = NS) and greater than in patients with CAD (1.78 +/- 0.76 ml/g/min; p < 0.05). However in patients with both syndrome X and CAD, MBF was more heterogeneous than in healthy subjects (48 +/- 12 and 48 +/- 11, respectively, vs 30 +/- 7; p < 0.01). Thus, in patients with syndrome X, MBF is abnormally heterogeneous both at baseline and after dipyridamole. These findings are compatible with the presence of dynamic alterations of small coronary arteries. Because these alterations appear to be very sparse within the myocardium, they can be undetected when myocardial perfusion, function and metabolism are assessed using conventional methods that are unable to detect small myocardial regions.

Adult↗
PubMed1993

Variability of coronary blood flow reserve assessed by Doppler catheter after successful thrombolysis in patients with acute myocardial infarction.

To establish whether abnormal function of small coronary vessels might limit the advantages of thrombolytic treatment, coronary flow reserve in the infarct-related artery was measured in nine patients with acute myocardial infarction early after successful coronary thrombolysis by using a Doppler catheter and intracoronary adenosine infusion. In each patient coronary flow reserve was calculated as the ratio between coronary blood flow velocity during the highest tolerated intracoronary dose of adenosine (0.5 mg/min in five patients and 1 mg/min in four patients) and baseline velocity. Coronary flow reserve ranged from 1 to 3 (mean 2 +/- 0.7). No correlation (r = 0.20; p = 0.58) was found between coronary flow reserve and the severity of residual coronary stenosis, which ranged between 23% and 76% (mean 47% +/- 17%). No correlation (r = 0.33; p = 0.39) was found between either coronary flow reserve and the interval between pain onset and administration of the thrombolytic treatment, which ranged between 2.2 and 6 hours (mean 4.2 +/- 1.4 hours). Thus, in patients with acute myocardial infarction, coronary flow reserve early after successful thrombolysis is strikingly variable and may be extremely low despite widely patent epicardial coronary arteries. This restriction of coronary blood flow, probably caused by abnormal function of small coronary vessels, might limit the potential benefit from successful coronary thrombolysis.

Adenosine↗
PubMed1993

Coronary vasomotor effects of serotonin in patients with angina. Relation to coronary stenosis morphology.

BACKGROUND: Previous experimental studies have shown that the effect of serotonin on a coronary stenosis depends on whether that stenosis is compliant or fixed. However, the relation between coronary stenosis morphology and the response to serotonin in patients with angina is not known. METHODS AND RESULTS: Using computerized quantitative coronary angiography, we studied the effects of intracoronary infusion of serotonin on 38 coronary stenoses of different morphologies (concentric, eccentric, complicated) in 11 patients with stable angina and 4 with variant angina. In response to the maximum infused concentration of serotonin, 100% of complicated stenoses and 50% of concentric stenoses constricted by > or = 20% (P < .05). The magnitude of constriction was greater at eccentric stenoses (32.08 +/- 4.1%) than concentric stenoses (15.68 +/- 2.8%, P < .05) and greater in complicated stenoses (57.69 +/- 7.6%, P < .05) than eccentric stenoses. At complicated stenoses, the constriction was greater (0.85 +/- 0.16 mm, P < .05) than at the adjacent reference segments (0.42 +/- 0.12 mm). It was similar to the reference segment for both concentric and eccentric stenoses. The constriction at the stenosis was greater for irregular (complicated) lesions than for smooth (concentric and eccentric) lesions in both patients with stable (51.8 +/- 7.3% versus 22.5 +/- 4.1%, P < .001) and those with variant (77 +/- 17% versus 28.2 +/- 8.1%, P < .05) angina. There was a weak correlation (r = .39) of magnitude of constriction with stenosis length but not with baseline stenosis severity (minimum diameter). CONCLUSIONS: In these patients, the magnitude of the vasoconstrictor response to serotonin at the site of an atheromatous coronary plaque depends on the morphological characteristics of the plaque and is more closely related to irregular contour than stenosis severity or length. This relation suggests that variations in receptor type or density or in the smooth muscle cell response to stimulation may determine the response to locally released serotonin in patients with coronary disease.

Angina Pectoris↗
PubMed1993

Patterns of coronary artery stenosis vasomotion: observed versus "predicted" stenosis reactivity in patients with chronic stable angina.

BACKGROUND: Patterns of constriction and dilatation of angiographically normal coronary artery segments and coronary stenoses, in response to vasoactive stimuli, remain speculative. METHODS: We compared the vasomotor response of angiographically normal and stenotic coronary segments and assessed the effects of stenosis location and morphology on coronary stenosis vasomotion in 52 patients with chronic stable angina (40 men and 12 women) who underwent intracoronary ergonovine or isosorbide dinitrate administration or both. Changes in coronary diameter in response to nitrate and ergonovine were assessed by computed arteriography. The "predicted" change in stenosis diameter was calculated according to the "geometric theory" (based on the vasomotor response of angiographically normal segments adjacent to the lesion and on stenosis severity). Coronary diameter was assessed at baseline and after nitrate administration in 58 stenoses (34 concentric and 24 eccentric), of which 40 were located proximally and 18 distally, and also after ergonovine administration (23 stenoses: 14 proximal and 9 distal, 14 concentric and 9 eccentric). RESULTS: Significant (> or = 10% lumen diameter change) vasoconstriction was observed after ergonovine administration in 14 of the 23 stenoses (61%), and significant vasodilation was noted after nitrate administration in 29 of 58 stenoses (50%). A larger proportion of distal (89%) and eccentric (89%) compared with proximal (43%) and concentric (43%) stenoses showed a greater than 10% vasoconstriction after ergonovine administration (P < 0.05). Vasodilatation after nitrate administration was also observed in a larger proportion of distal (78%) and eccentric (67%) than in proximal (38%) and concentric (38%) stenoses (P < 0.05). On average, the "observed" changes in coronary diameter in response to nitrate and ergonovine administration were of significantly less magnitude than those "predicted" by the geometric theory in both proximal and distal stenoses and in concentric and eccentric stenoses. In only 17% of stenoses were observed and predicted vasoconstriction similar. CONCLUSIONS: Our results suggest that in patients with chronic stable angina, calculations based on the "geometric theory" cannot predict the actual vasomotor response of a stenosis. Factors other than severity, such as baseline coronary tone, stenosis location, and stenosis morphology, appear to modulate stenosis vasomotion in vivo.

Adult↗
PubMed1993

Myocardial ischaemia in the hypertensive patient--the role of coronary microcirculation abnormalities.

Clinicians have long suspected that hypertrophied hearts have an inadequate coronary circulation. This clinical suspicion resulted from the observation that a large proportion of patients with left ventricular hypertrophy who have normal coronary arteriograms complain of angina and have ischaemia-like ST segment depression during effort. Hypertension is a known risk factor for the development of coronary artery disease and therefore the presence of angina in a patient with systemic hypertension is usually attributed to obstructive atherosclerotic coronary artery disease. However, angina may occur in hypertensive patients in the absence of coronary stenosis. A limitation of coronary flow reserve is responsible for signs and symptoms of myocardial ischaemia in many of these patients. This article will focus on the role of the coronary microcirculation in the genesis of ischaemia in patients with systemic hypertension who have no obstructive coronary artery disease. It will also briefly discuss other mechanisms potentially responsible for the angina syndrome in patients who have left ventricular hypertrophy but angiographically normal coronary arteries.

Angina Pectoris↗
PubMed1992

Preangioplasty complicated coronary stenosis morphology as a predictor of restenosis.

To assess whether complicated preangioplasty coronary stenosis morphology is associated with restenosis, 41 patients (47 stenoses) who underwent repeat angiography 6 to 8 months after percutaneous transluminal coronary angioplasty (PTCA) were studied. Stenosis diameter and morphology were assessed by computerized quantitative coronary angiography before and immediately after PTCA and at follow-up angiography. Before PTCA 18 stenoses were concentric (symmetric narrowings with smooth borders), 12 were eccentric (asymmetric narrowings with smooth borders), and 17 were complicated (asymmetric with rough borders and overhanging edges). Restenosis occurred in 18 lesions: two (11%) concentric, four (33%) eccentric, and 12 (70%) complicated (p less than 0.05), whereas 29 lesions remained unchanged. Stenosis diameter before and immediately after PTCA was not significantly different in the 18 patients with and the 23 patients without restenosis. Follow-up angiograms showed that 11 (61%) stenoses in the group with restenosis and 18 (63%) in the group without restenosis had morphology similar to that before PTCA. Restenosis occurred in seven (30%) patients who initially had chronic stable angina and in 11 (61%) who were first seen with unstable angina (p less than 0.05). In patients with stable angina 1 of 13 concentric stenoses, two of eight eccentric stenoses, and four of five complicated lesions restenosed. In patients with unstable angina one of five concentric, two of four eccentric, and 8 of 12 complicated lesions had restenosis. Stenoses that were complicated before PTCA tended to adopt an irregular morphology if they recurred, whereas concentric stenoses rarely occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

A combination of electrocardiographic methods represents a further step toward the noninvasive identification of patients with syndrome X.

Identification of patients with angina but normal coronary arteriograms (syndrome X) using noninvasive means would be desirable. The ability of four established exercise electrocardiographic methods to identify angina patients with and without coronary artery disease was compared with that of a method based on a combination of the above (combined method). A treadmill score, a multivariate method, the ST segment recovery loop, the ST/heart rate adjustment, and the combined method were applied to 112 patients who had typical exertional angina and positive exercise tests (greater than 1 mm ST segment depression); 90 had documented coronary artery disease and 22 had syndrome X. The combined method and the treadmill score had a significantly higher diagnostic accuracy (both 81%, as 91 of the 112 patients were correctly identified by both methods) than the multivariate (66%) and ST segment recovery loop (64%) methods (p less than 0.05). The ST/heart rate adjustment had a lower sensitivity for syndrome X than any other method (1 of 22). Thus methods that involve the assessment of both ST and non ST segment variables have greater accuracy in separating syndrome X and coronary artery disease patients than methods relying more heavily on ST segment changes.

Adrenergic beta-Antagonists↗
PubMed1992

Relation between stimulation site of cardiac afferent nerves by adenosine and distribution of cardiac pain: results of a study in patients with stable angina.

OBJECTIVES: The purpose of this study was to establish whether stimulation of cardiac sensory receptors in different myocardial regions results in different distributions of cardiac pain. BACKGROUND: Previous studies have shown that adenosine provokes cardiac pain through stimulation of sensory receptors in the absence of myocardial ischemia. In this study adenosine was used to obtain a regional stimulation of cardiac sensory receptors. METHODS: Increasing doses of adenosine (0.25, 0.5 and 1 mg/min) were selectively infused into the right and then into the left coronary artery in 26 patients with stable angina. RESULTS: No patient developed ischemic electrocardiographic changes during either adenosine infusion. Eighteen patients experienced cardiac pain during both infusions. Despite the stimulation of sensory receptors in different myocardial regions, 13 patients experienced cardiac pain in the same body area. Adenosine-induced pain was always similar to the anginal pain. By contrast, the remaining five patients experienced adenosine-induced cardiac pain in different body areas. In two of these patients, the distribution of anginal pain was similar to that experienced during one of the two adenosine infusions. In the remaining three patients, the distribution of anginal pain was similar to that experienced during adenosine infusion into the right coronary artery during some anginal episodes and to that experienced during adenosine infusion into the left coronary artery during other episodes. CONCLUSIONS: During stimulation by adenosine of sensory receptors in different myocardial regions, the majority of patients experience cardiac pain in the same body area; only a few experience pain in different areas. These differences might be caused by different organizations of the ascending neural pathways to the cortex. Our results suggest that in the same patient different distributions of pain during anginal attacks are probably due to ischemia in different myocardial regions.

Adenosine↗
PubMed1992

Variant angina pectoris. Role of coronary spasm in the development of fixed coronary obstructions.

BACKGROUND: It has been suggested that recurring coronary artery spasm may lead to the development of fixed atherosclerotic coronary obstructions. METHODS AND RESULTS: We studied 10 patients with typical Prinzmetal's variant angina in whom the disease remained active for years and in whom occlusive coronary spasm occurred reproducibly at the same arterial site during repeat coronary arteriography (25 +/- 12 months after initial angiography). At initial evaluation, four patients had significant (greater than or equal to 50% fixed coronary diameter reduction) one-vessel coronary artery disease, and six had nonsignificant disease. Spasm developed at stenotic sites (20-65% diameter reduction) in nine patients and at an angiographically normal site in one patient. Progression of coronary disease was assessed in 62 segments: 10 spastic (of which nine were stenotic) and 52 nonspastic (eight stenotic and 44 angiographically normal), using computerized arteriography. Mean diameters (millimeters) of spastic segments, nonspastic stenoses, and angiographically normal nonspastic segments were not significantly different at first and second arteriograms (1.52 +/- 0.14 versus 1.43 +/- 0.21, 1.32 +/- 0.17 versus 1.12 +/- 0.23, and 2.40 +/- 0.12 versus 2.42 +/- 0.12, respectively). Stenosis progression (from 65% diameter reduction to total occlusion) occurred in one patient at a spastic site and in two at nonspastic sites (from 34% to 65% and from 84% to 100%). Complicated stenoses suggestive of plaque fissuring were not observed during the study. CONCLUSIONS: In patients with chronic Prinzmetal's variant angina without myocardial infarction, stenosis progression was not frequently observed at spastic sites despite the recurrence of focal coronary spasm over relatively long periods of time.

Adult↗
PubMed1991

Absence of myocardial dysfunction during stress in patients with syndrome X.

Stress two-dimensional echocardiographic studies were performed in 18 patients with angina, a positive exercise test and normal findings on coronary angiography (syndrome X). Rest and immediate posttreadmill exercise two-dimensional echocardiograms were performed with a digitized cine loop and side by side visual analysis in all patients. In 16 of these patients, right atrial pacing up to 160 beats/min was also performed and percent systolic wall thickening was calculated at five equally spaced segments around the left ventricle, each corresponding to an anterior, lateral and inferior wall and the posterior and the anterior ventricular septum. Measurements of percent systolic wall thickening were established in 10 age- and gender-matched normal persons for comparison. ST segment depression occurred in all patients during exercise and persisted for 42.1 s (range 18 to 75) into the recovery period. Immediate postexercise echocardiography was started within 20.1 +/- 5.4 s and completed in 54.1 +/- 11.3 s. No patient had regional wall motion abnormalities seen on two-dimensional imaging of any myocardial segment. Thirteen patients (72%) reported reproduction of their usual chest pain, which led to termination of the test. During rapid right atrial pacing, nine patients (56%) developed ST segment depression that was associated with angina in seven. In all 16 patients, percent systolic wall thickening increased over values at rest in each myocardial segment. Percent systolic wall thickening averaged 47.1 +/- 6.1% at rest and increased to 74 +/- 8% during right atrial pacing (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗