Enhanced vasomotor responses of complex coronary stenoses to acetylcholine in stable angina pectoris.
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Acetylcholine↗
Biomedical subjects
J C Kaski
Publications and source records attributed to J C Kaski.
Differential progression of complex and smooth stenoses within the same coronary tree in men with stable coronary artery disease.
OBJECTIVES: We sought to compare the evolution of complex and smooth stenoses within the same coronary tree in patients with stable coronary artery disease. BACKGROUND: Progression of coronary stenosis has prognostic significance and may be influenced by local and systemic factors. Stenosis morphology is a determinant of disease progression, but no previous study has systematically assessed progression of complex and smooth stenoses within the same patient. METHODS: We studied 50 men with stable angina who 1) had one complex coronary stenosis and one smooth stenosis in different noninfarct-related coronary vessels at initial coronary angiography, and 2) had a second angiogram after a median interval of 9 months (range 3 to 24). Patients with lesions > or = 10 mm long, at a major branching point or with > 85% diameter reduction were not included. Coronary lesions were measured quantitatively from comparable end-diastolic frames. Stenosis morphology was determined qualitatively by two independent observers. RESULTS: All patients remained in stable condition during follow-up. Progression, defined as an increase in diameter stenosis by > or = 15% was seen in only eight complex stenosis (16%) but in no smooth lesions (p < 0.01). The severity of complex stenoses changed more than that of corresponding smooth stenoses (mean +/- 1 SD 5.8 +/- 13% vs. -0.06 +/- 6%, p < 0.01). On average, the annual rate of growth was 11.4 +/- 28% and 1.5 +/- 14% for complex and smooth lesions, respectively (p < 0.01). CONCLUSIONS: Few coronary stenoses progress rapidly in stable angina. Complex and smooth coronary stenoses progress at different rates within the same coronary tree. complex stenosis morphology itself is an important determinant of progression of stenosis in patients with apparently clinically stable coronary artery disease.
Aged↗
Cardiac syndrome X: clinical characteristics and left ventricular function. Long-term follow-up study.
OBJECTIVES: Our aim was to study the clinical characteristics and evolution of symptoms and left ventricular function in a clinically homogeneous group of patients with syndrome X (angina pectoris, positive exercise test results and normal coronary arteriograms). BACKGROUND: The syndrome of angina with normal coronary arteriograms is heterogeneous and encompasses different pathogenetic entities. These characteristics may contribute to the existing controversy concerning the cause of syndrome X. METHODS: We studied 99 patients with syndrome X (78 women, 21 men; mean age +/- SD 48.5 +/- 8 years). All underwent clinical characterization, ambulatory electrocardiographic (ECG) monitoring and echocardiographic assessment of left ventricular function during a follow-up period of 7 +/- 4 years. RESULTS: The syndrome was more common in women than in men. Of the women, 61.5% were postmenopausal before the onset of chest pain. All 99 patients had exertional angina, and 41 also had rest angina. The average duration of episodes of chest pain was > 10 min in 53% of patients. Sublingual nitrate was effective for relief of pain in 42% of patients. Transient ST segment depression was observed during ambulatory ECG monitoring in 64 patients and myocardial perfusion abnormalities in 22. During the first stage of the exercise test, 32 patients had an increase > 20 mm Hg in systolic blood pressure and showed an earlier onset of ST depression and shorter exercise time than did patients whose blood pressure increased < or = 20%. During follow-up, no deaths or myocardial infarctions occurred, ventricular function was unchanged (shortening fraction 35.4 +/- 4% vs. 35.6 +/- 3%; heart failure developed in only one patient), systemic hypertension occurred in eight patients and conduction disturbances in four. Symptoms lessened in 11 patients, were variable or unchanged in 64 and worsened in 24. CONCLUSIONS: Syndrome X, as defined in this study, occurs predominantly in postmenopausal women. Patients usually have chest pain typical for angina, but conventional antianginal treatment is not often successful. Myocardial perfusion abnormalities occur in a small proportion of patients. Long-term survival is not adversely affected, and deterioration of cardiac function rarely occurs.
Adult↗
Abnormal uptake and washout of thallium-201 in patients with syndrome X and normal-appearing scans.
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Age Factors↗
Management of vasospastic angina--role of nicorandil.
Clinical and experimental observations have confirmed that an episodic increase in the vasomotor tone of a major coronary artery may play a pathogenetic role not only in "variant angina" but also in other, more common anginal syndromes. In chronic stable angina, dynamic changes of vascular smooth muscle tone at the site of eccentric atheromatous plaques are responsible for "mixed angina." Abnormal coronary vasomotion contributes to myocardial ischemia in acute coronary syndromes as well. Studies have shown that a "primary" reduction of coronary blood flow, usually associated with plaque fissuring and thrombus formation, causes infarction and unstable angina. Abnormal vasoconstriction associated with the release of vasoactive substances by platelets and other constituents of the thrombus can contribute to coronary flow reduction in patients with unstable angina and myocardial infarction. Better understanding of the complex interactions among atherosclerotic coronary obstructions, the vascular smooth muscle, and the vascular endothelium has resulted in novel therapeutic approaches and has stimulated the search for more efficacious and safer coronary vasodilators. Recently interest has focused on vasodilator agents such as nicorandil that influence coronary arterial tone by acting through potassium channel activation. Nicorandil appears to be effective for treatment of vasospastic angina, as suggested by studies in Japan and Europe. In addition to its "antivasospastic" properties, nicorandil dilates coronary artery stenoses in patients with stable angina pectoris.(ABSTRACT TRUNCATED AT 250 WORDS)
Angina Pectoris↗
Heart rate variability depression in patients with unstable angina.
The degree of reduction in heart rate variability (HRV) after myocardial infarction has been shown to have prognostic significance, but HRV has not been studied extensively in patients with unstable angina. We assessed spectral and nonspectral measurements of HRV in 52 patients with unstable angina, 52 patients with acute myocardial infarction, and 41 normal subjects. The spectral bands of 0.04 to 0.15 Hz (low frequency), 0.15 to 0.4 (high frequency), and nonspectral parameters SDNN, SDANN, SDNN index, rMSSD, and pNN50 were calculated from continuous 24-hour ECGs. All measures of HRV were reduced in patients with acute coronary syndromes compared to normal controls (p < 0.001), and there was no significant difference in measure of HRV between unstable angina and myocardial infarction patients. In patients with unstable angina who stabilized after admission, HRV had increased by the second 24 hours of monitoring. In contrast, HRV was further depressed in patients who had episodes of chest pain or transient ST-segment depression during the second 24 hours. rMSSD, pNN50, and SDNN index were lower in patients with unstable angina who had transient silent ischemia compared to those without silent ischemia. Of the patients with unstable angina, 4 died and 1 had nonfatal acute myocardial infarction within 11 months. HRV was lower in these patients than in patients without further cardiac events.
Aged↗
Rapid angiographic progression of "target" and "nontarget" stenoses in patients awaiting coronary angioplasty.
OBJECTIVES: Our aim was to compare the short-term evolution of "target" versus "nontarget" stenoses in patients awaiting coronary angioplasty. BACKGROUND: Coronary angioplasty is effective therapy for angina pectoris, but coronary events occur after successful angioplasty that are caused by both restenosis and progression of mild preexisting nontarget stenoses. METHODS: We prospectively studied 161 consecutive patients with stable angina (124 men and 37 women). After diagnostic angiography, target stenoses for angioplasty and nontarget lesions were identified. Patients were put on a routine waiting list and followed up regularly until repeat coronary arteriography was performed (mean +/- SD 7 +/- 3 months), either immediately before angioplasty (138 patients) or soon after an acute coronary event (23 patients), if one occurred. Stenosis diameter was measured by using computerized arteriography. Progression of disease was defined as > or = 20% lesion diameter reduction, new total occlusion or development of a "new" stenosis > or = 30%. RESULTS: At study entry, the mean diameter of target (n = 207) and nontarget (n = 184) lesions was 68 +/- 9% and 38 +/- 9%, respectively (p < 0.001). Disease progression occurred in 33 patients (20%). Seven new lesions (one total occlusion) developed. Eighteen target (9%) and 15 nontarget (8%) stenoses progressed. The power of the study to detect a difference of 1% between the risks of progression of target and nontarget stenoses with a 90% probability was < 0.1. Total occlusion developed in 15 (83%) of the 18 target and 6 (40%) of the 15 nontarget stenoses (p = 0.03). During follow-up, a myocardial infarction developed in 3 patients (2%) and unstable angina in 20 (12%). These coronary events were associated with progression of target stenoses in 10 patients and nontarget stenoses in 7 and with the development of new lesions in 1. In five patients coronary events were not associated with stenosis progression. CONCLUSIONS: Despite differences in baseline severity, a similar proportion of target and nontarget lesions progressed rapidly. However, target stenoses were more likely than nontarget lesions to progress to total occlusion. Progression of nontarget stenoses may contribute to recurrence of angina and new coronary events after successful angioplasty and should be considered when developing strategies aimed at improving outcome after angioplasty.
Aged↗
The relationship between change and initial value: the continuing problem of regression to the mean.
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Coronary Disease↗
Syndrome X in women is associated with oestrogen deficiency.
This study was undertaken to ascertain whether gynaecological history or a reduction in ovarian hormones are triggers of angina in menopausal women with a positive exercise test and normal coronary arteries. The majority of patients with angina pectoris, a positive exercise test and normal coronary arteries are female, suggesting that the female gender may be important in the aetiology. We studied the gynaecological features of 107 women (age 53 +/- 9 years) with syndrome X, taken from a population of 134 patients including 27 males. Cardiological investigations were undertaken and detailed gynaecological history obtained from all the female patients. Menopausal status was confirmed by plasma levels of oestradiol-17 beta < or = 100 pmol.l-1. In 95 of the 107 female patients, chest pain began either during the perimenopausal period (32) or after the menopause (63). Of the 63 menopausal patients, 43 had undergone hysterectomy at an average of 8 +/- 6 years prior to the onset of chest pain. The incidence of hysterectomy in the study population (40%) was four times greater than that of an age-matched population. These findings confirm that the majority of patients with syndrome X are women in whom the chest pain began after the onset of menopause. Ovarian hormone deficiency may, therefore, play a role in the onset of syndrome X in female patients.
Adult↗
Aggressive pattern of angina after successful coronary angioplasty: the role of clinical and angiographic factors.
To assess possible clinical and angiographic factors associated with acute coronary events following PTCA, we performed quantitative angiography in 168 consecutive patients who had undergone successful angioplasty in a native vessel (94 for stable angina, 74 for unstable angina), and who were restudied (24 +/- 15 weeks; range 4 to 52) because of recurrent anginal symptoms. Of the 168 patients, 38 (Group 1) were restudied because the pattern of angina was aggressive (unstable angina in 31, myocardial infarction in 7) and 130 because of effort-related angina (Group 2). the two patient groups were well matched for extent of initial disease but patients in Group 1 were younger (P=0.03). PTCA for unstable angina was originally performed more frequently in Group 1 than in Group 2 (27 of 38 patients (71% vs 47 of 130 patients (36%), P=0.0004). Disease progression in non-dilated segments occurred in 10 patients (26%) in Group 1 compared with eight (6%) in Group 2 (P=0.0004). Disease progression in non-dilated segments occurred in nine patients (24%) in Group 1 and in Group 2 (P=0.0004). Disease progression in non-dilated segments occurred in nine patients (24%) in Group 1 and in 10 (8%) in Group 2 (P=0.0006). Our conclusion is that patients who require re-investigation as a result of angina which has become aggressive following PTCA are usually those who originally underwent PTCA for unstable angina. These patients have a higher incidence of occlusive restenosis or disease progression.
Adult↗
Identification of patients at high risk for adverse coronary events while awaiting routine coronary angioplasty.
BACKGROUND: Identification of patients at risk for progression of coronary stenosis and adverse clinical events while awaiting coronary angioplasty is desirable. OBJECTIVE: To determine the standard clinical or angiographic variables, or both, present at initial angiography associated with the development of adverse coronary events (unstable angina, myocardial infarction, and angiographic total coronary occlusion) in patients awaiting routine percutaneous transluminal coronary angioplasty (PTCA). PATIENTS AND METHODS: Consecutive male patients on a waiting list for routine PTCA. Routine clinical details were obtained at initial angiography. Stenosis severity was measured using computerised angiography. OUTCOME MEASURES: Development of one or more of myocardial infarction, unstable angina, or angiographic total coronary occlusion while awaiting PTCA were recorded as an adverse event. RESULTS: Some 214 of 219 patients underwent a second angiogram. One had a fatal myocardial infarction and four (2%) were lost to follow up. Fifty patients (23%) developed one or more adverse events (myocardial infarction five, unstable angina 35, total coronary occlusion 23) at a median (range) interval of 8 (3-25) months. Twenty (57%) of the 35 patients with unstable angina developed adverse events compared with 30 (17%) of the 180 with stable angina (P = 0.0001). Plasma triglyceride concentration was 2.6 (1.2) mmol/l in patients with adverse coronary events compared with 2.2 (1.1) mmol/l in those without such events (P < 0.05). Patients with adverse events were younger than those without (54 (9) years v 58 (9) years, P < 0.01). The relative risk of an adverse event in patients with unstable angina and increased plasma triglyceride concentrations was 6.9 compared with those presenting with stable angina and a normal triglyceride concentration (P < 0.02). CONCLUSIONS: The study shows that adverse events are not uncommon in patients awaiting PTCA. Patients at high risk for adverse events may be predicted by the presence of acute coronary syndrome, increased concentration of plasma triglyceride, and younger age at the time of the first angiogram.
Adult↗
Concentration of circulating plasma endothelin in patients with angina and normal coronary angiograms.
BACKGROUND: Some patients with angina pectoris and normal coronary arteriograms have reduced coronary flow reserve and abnormal endothelium dependent vasodilator responses. Endothelin-1 (ET-1), a potent vasoconstrictor, is an important modulator of microvascular function and may also have algogenic properties. METHOD: Plasma ET-1 was measured in peripheral venous blood in 40 patients (30 women) (mean (SD) age 56 (8) years) with angina and normal coronary arteriograms and 21 normal controls (17 women) (mean (SD) age 53 (7) years). Patients with systemic hypertension, left ventricular hypertrophy, or coronary spasm were excluded. Plasma ET-1 was measured using radioimmunoassay. RESULTS: Thirty five patients had > or = 1 mm ST segment depression during exercise. Left bundle branch block was present in four patients at rest and in one during exercise. Mean (SD) (range) concentration of ET-1 (pg/ml) was higher in patients than in controls (3.84 (1.25) (1.97-7.42) v 2.88 (0.71) (1.57-4.48) P < 0.0001). In patients with "high" (> control mean (one SD)) ET-1 concentrations (n = 23), the time to onset of chest pain during exercise was significantly shorter (6.21 (3.9) v 9.03 (3.9) min; p = 0.01) than in patients with "low" ET-1 concentrations. Of the five patients with left bundle branch block, four had plasma ET-1 concentration > 4.0 pg/ml. CONCLUSION: Plasma endothelin is raised in patients with angina and normal coronary arteriograms and is consistent with the demonstration of endothelial dysfunction in such patients. The association between "high" plasma ET-1 and an earlier onset of chest pain during exercise suggests that endothelin may also have a role in the genesis of chest pain in patients with normal coronary arteries.
Adult↗
Clinical factors and angiographic features associated with premature coronary artery disease.
BACKGROUND: Clinical, angiographic, and biochemical features may differ in young patients with coronary heart disease compared with older patients. METHODS: We compared clinical and angiographic characteristics in 100 male patients with clinical onset of disease at age < or = 45 years (group 1) with those of 100 older male patients (clinical onset of disease at > or = 60 years) (group 2). All patients had documented coronary artery disease. The two patient groups were compared in terms of the pattern of angina at disease onset, angiographic features, and coronary risk factors. RESULTS: Seventy-six patients in group 1 and 49 patients in group 2 presented with acute coronary syndromes (unstable angina or myocardial infarction) at clinical disease onset (p < 0.001). Compared with patients in group 2, younger patients (group 1) showed a preponderance of single-vessel disease (54 vs 36%; p < 0.001) and complex stenosis morphologic features (59 vs 36%; p < 0.01). Family history of coronary artery disease (39 vs 11%; p < 0.001) and smoking (73 vs 46%; p < 0.001) were also more prevalent in younger patients. Mean plasma total cholesterol level was 6.4 +/- 1.3 mmol/L in group 1 and 6.1 +/- 1.2 mmol/L in group 2 (p = NS). Younger patients, however, had lower high-density lipoprotein (HDL) cholesterol (0.9 +/- 0.2 mmol/L and 1.1 +/- 0.4 mmol/L; p < 0.01) and higher plasma triglyceride levels compared with patients of group 2 (2.7 +/- 1.3 mmol/L vs 2.1 +/- 1.1 mmol/L; p < 0.001). CONCLUSIONS: Patients with premature coronary disease referred to coronary angiography commonly have unheralded acute onset of symptoms, angiographically complex stenosis morphologic features, and less extensive coronary artery disease. In addition to previously identified risk factors such as family history and smoking, we observed that high plasma triglyceride and low HDL cholesterol levels are associated with premature coronary artery disease.
Adult↗
[The diagnosis of myocardial damage during coronary angioplasty by the analysis of the isoforms of the enzyme creatine kinase MB].
BACKGROUND: The existence of myocardial damage during percutaneous transluminal coronary angioplasty (PTCA) is controversial. Mild elevations in creatine kinase (CK) activity and its isoenzyme MB (CKMB) in patients who underwent PTCA have been reported. However, other authors failed to confirm these elevations. The low sensitivity of total CK and CKMB activity for the detection of myocardial damage in different settings other than myocardial infarction might account for the controversial findings. Measurement of CKMB isoforms has been shown to have a higher sensitivity than the assessment of CK or CKMB activity for early diagnosis of myocardial infarction. Its sensitivity for the diagnosis of myocardial damage in settings other than infarction is not well described. OBJECTIVES: The aim of our study was two-fold: 1) to assess the incidence of myocardial damage after PTCA and 2) to compare the sensitivity of total CK and CKMB activity and measurement of CKMB isoforms for the detection of myocardial damage. METHODS: 14 patients (11 men and 3 women) with chronic stable angina underwent PTCA. Two electrocardiographic leads were monitored from the beginning of the procedure until 30 minutes after the PTCA. ST segment shifts of at least 1 mm, lasting for more than 1 minute, were considered indicative of myocardial ischemia. The duration of ischemic episodes was measured from the onset of the ST shift until its return to baseline. Total ischemic time, in minutes, was the sum of the duration of every ischemic episode. Blood samples were drawn before PTCA and serially during the first 24 hours post PTCA. CK (normal < 200 U/l) and CKMB (normal < 14 U/l) activities were measured. The CKMB isoforms were separated by electrophoresis, measured by densitometric scanning and their ratio calculated (CKMB2/CKMB1 normal < 1.5). RESULTS: Vessels which underwent PTCA were: the left anterior descending artery (LDA) in 5 patients, the circumflex coronary artery (Cx) in 3 patients, right coronary artery (RCA) in 3 patients, LDA and Cx in 1 patient and Cx and RCA in 2 cases. Eleven patients underwent balloon dilatation, 1 underwent atherectomy (Rotablator) and two patients had treatment with both Rotablator and balloon angioplasty. Ischemic ST segment shifts were found in ten patients and the median of total ischemic time was 13.5 minutes (interquartile range: 2-15 minutes). Total CK and CKMB activities were within the normal range in every patient whereas in 7 patients (50%) the peak ratio CKMB2/CKMB1 was above the normal range. There were no differences in age, sex, number of vessels or lesions treated or in the time of balloon inflation between patients with and without abnormal CKMB2/CKMB1 peak. However, the ischemic time was significantly higher in patients with CKMB2/CKMB1 > 1.5 (median 15 vs 0 minutes; p = 0.023). CONCLUSIONS: Myocardial damage during PTCA is not an uncommon finding. The CKMB isoforms are more sensitive markers of myocardial damage during PTCA than total CK or CKMB activities.
Aged↗
Regional variations in ETA/ETB binding sites in human coronary vasculature.
Endothelin (ET)-1 is an endothelium-derived constrictor peptide that is believed to play a pathophysiologic role in coronary artery disease. Receptors for this peptide have been identified on human coronary tissue by in vitro autoradiography. A number of available compounds are selective for ETA or ETB receptors. Here we have used radiolabeled PD 151242 and BQ 3020 to identify ETA and ETB binding sites on sections of human coronary vasculature. ETA receptors are associated with smooth muscle of the coronary artery. Smooth muscle ETB receptor binding is weak at proximal portions of this vessel but increases toward distal regions. ETB receptors are exclusively associated with myocardial capillaries. Our results indicate that, apart from ETA-induced vasoconstriction, stimulation of ETB receptors at distal regions of the coronary vasculature and myocardial microvessels may play an important role in the pathophysiology of coronary syndromes.
Autoradiography↗
[3H]bosentan binding to human coronary artery: functional correlates.
The binding characteristics and localization of bosentan, an orally active endothelin-1 (ET-1) antagonist, were studied on sections of human coronary artery by in vitro autoradiography. Competition studies were performed to determine the ability of bosentan to prevent [125I]ET-1 binding to the coronary vasculature. The effects of bosentan on ET-1-induced contraction of the coronary artery were also studied in vitro. [3H]Bosentan bound to the tunica media of the human coronary artery. Unlabeled bosentan prevented [125I]ET-1 binding to this vessel in a concentration-dependent manner, and functional studies indicated that bosentan antagonizes ET-1--induced constriction. These data show that bosentan is able to reduce ET-1 binding to the human coronary artery and ET-1 constrictor effects in vitro. Bosentan is an orally active ET-1 antagonist, and these results suggest that this compound might be used to block the effects of locally released ET-1 in pathologic conditions, such as atherosclerosis, angina, and myocardial ischemia.
Autoradiography↗
Endothelin-like immunoreactivity in atherosclerotic human coronary arteries.
Endothelin-1 (ET-1) is an endothelium-derived peptide with powerful vasoconstrictor and mitogenic properties. A pathophysiologic role for ET-1 has been suggested, because increased plasma and tissue levels of this peptide have been described in a number of disease states, including atherosclerosis. Immunocytochemistry was carried out on sections of coronary arteries from patients undergoing cardiac transplantation to identify regions exhibiting ET-1-like immunoreactivity (ET-LI). ET-LI was associated with endothelial cells of the lumen and with microvascular endothelial cells of the adventitia, regions of neovascularization, and recanalization within atherosclerotic plaques. ET-LI was observed in the tunica media, and patches of immunostaining were also associated with smooth-muscle cells within the plaque. These results indicate that ET-1 not only is released from the vascular endothelium but, under certain conditions, is also generated by smooth muscle cells. An autocrine action of ET-1 is well established, and our results suggest that this peptide is involved in neovascularization and smooth-muscle cell proliferation associated with atherosclerosis.
Coronary Artery Disease↗
"Syndrome X" as a consequence of acute myocardial infarction.
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Adult↗