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PubMed1995

Selective ergonovine-induced coronary artery spasm and ST-segment alternans after blunt thoracic trauma.

A 24-year-old man was found to have angiographically normal coronary arteries shortly after suffering blunt thoracic trauma. Selective ergonovine administration into the left coronary artery induced total occlusion of the left anterior descending branch and electrical alternans of the ST-segment. This case demonstrates coronary artery spasm as a possible mechanism of coronary occlusion after blunt thoracic trauma.

Adult↗
PubMed1994

Long-term follow-up of coronary narrowing with spasm.

In order to clarify the fate of coronary narrowing with spasm, repeat angiograms of coronary narrowing with and without spasm were compared. The mean interval between the first and second angiograms was 3.6 years (range, 1.1-8.5 years). Improvement of narrowing was more frequent in the vasospastic group (23%) than in the group without spasm (3%, P < 0.005). The cause of this improvement in the vasospastic group may have been the resolution of the spasm in the first angiogram, but the presence of intravascular thrombus or bleeding or edema of the coronary arterial wall may have resolved in the second angiogram.

Angina Pectoris, Variant↗
PubMed1988

Circulating cardiac myosin light chains in patients with angina at rest: identification of a high risk subgroup.

To detect myocardial cell damage, serum samples of 42 consecutive patients with angina at rest were screened for cardiac myosin light chains, which were detected in 22 patients (52%). In 17 of these patients there was a persistent release of myosin light chains lasting until the 4th hospital day, whereas in 7 patients myosin light chains were only detectable during the initial 24 h after admission. The presence of myosin light chains correlated with signs of ischemia in the electrocardiogram (ECG) (p less than 0.05) and with the extent of coronary artery narrowing (p less than 0.05). Cardiac myosin light chains were elevated in serum only if there was a greater than or equal to 75% diameter narrowing in at least one major vessel. In all five patients who developed transmural myocardial infarction during the course of their hospital stay, myosin light chains were detectable greater than or equal to 28 h before the diagnosis of myocardial infarction could be established by ECG criteria and conventional serum enzymes. Thus the detection of circulating cardiac myosin light chains enables one to identify a subgroup of patients with angina at rest having more severe coronary artery disease with a worse outcome.

Adult↗
PubMed1992

Endothelium-dependent dilator response to substance P in patients with coronary spastic angina.

OBJECTIVE: This study was designed to examine whether patients with coronary spastic angina have an impaired coronary artery dilator response to substance P, an endothelium-dependent vasodilator. BACKGROUND: Impairment of the endothelium-dependent vasodilator response has been suggested to be involved in the pathogenesis of coronary spasm. METHODS: In 11 patients with coronary spastic angina and 11 control patients, substance P was infused into the coronary artery at 20 pmol/min for 5 min. Incremental doses of acetylcholine were then injected into the coronary artery. The effects of these drugs and nitroglycerin on the coronary artery diameter were quantitatively analyzed. RESULTS: Heart rate, systolic blood pressure and rate-pressure product did not change after substance P infusion. In 12 coronary arteries of the patients with coronary spastic angina, spasm was induced with acetylcholine. At the site of coronary spasm documented, the lumen diameter, which was 1.6 +/- 0.5 mm at baseline, increased to 2.1 +/- 0.7 mm after substance P infusion (p less than 0.01). It decreased to 0.2 +/- 0.3 mm during acetylcholine-induced spasm (p less than 0.001) and increased to 2.3 +/- 0.8 mm after nitroglycerin administration (p less than 0.001 vs. baseline and p = NS vs. after substance P infusion). Of the 12 arteries with spasm, 5 were angiographically normal and the other 7 were minimally or moderately atherosclerotic: the diameter change after substance P was +28 +/- 20% and +30 +/- 22%, respectively (p = NS). In control patients, the diameter of the middle portion of the left anterior descending artery, which was 2.0 +/- 0.4 mm at baseline, increased to 2.5 +/- 0.4 mm after substance P infusion (p less than 0.001). The diameter changes after substance P infusion were not different between the patients with coronary spastic angina and control patients. CONCLUSIONS: Substance P dilated the artery with spasm of the patients with coronary spastic angina to a degree similar to that in control patients, indicating the preserved endothelium-dependent dilator response at the site of coronary spasm by way of substance P receptor.

Acetylcholine↗
PubMed1993

Randomized placebo-controlled trial of amlodipine in vasospastic angina. Amlodipine Study 160 Group.

OBJECTIVES: This study was designed to assess the efficacy and safety of amlodipine, a long-acting calcium channel blocker, in patients with vasospastic angina. BACKGROUND: Previous studies have established the value of short-acting calcium channel blockers in the treatment of coronary spasm. METHODS: Fifty-two patients with well documented vasospastic angina were entered into the present study. After a single-blind placebo run-in period, patients were randomized (in a double-blind protocol) to receive either amlodipine (10 mg) or placebo every morning for 4 weeks. Twenty-four patients received amlodipine and 28 received placebo. All patients were given diaries in which to record both the frequency, severity, duration and circumstances of anginal episodes and their intake of sublingual nitroglycerin tablets. RESULTS: The rate of anginal episodes decreased significantly (p = 0.009) with amlodipine treatment compared with placebo and the intake of nitroglycerin tablets showed a similar trend. Peripheral edema was the only adverse event seen more frequently in amlodipine-treated patients. No patient was withdrawn from the double-blind phase of the study because of an adverse event. Patients who completed the double-blind phase as responders to amlodipine or as nonresponders to placebo were offered the option of receiving amlodipine in a long-term, open label extension phase. During the extension, the daily dose of amlodipine was adjusted to 5 or 15 mg if needed and the rate of both anginal episodes and nitroglycerin tablet consumption showed statistically significant decreases between baseline and final assessment. CONCLUSION: This study suggests that amlodipine given once daily is efficacious and safe in the treatment of vasospastic angina.

Adult↗
PubMed1993

Increased echodensity of transiently asynergic myocardium in humans: a novel echocardiographic sign of myocardial ischemia.

OBJECTIVES: This study was conducted to establish whether changes in myocardial texture can be observed in humans by transthoracic echocardiography during ischemic episodes of different severity and duration induced by various pathogenetic mechanisms. BACKGROUND: Increased echo-reflectivity of ischemic myocardium has been detected in experimental animals by epicardial echocardiography and by backscatter evaluation. METHODS: Transthoracic two-dimensional echocardiographic monitoring with a commercially available electronic sector scanner (2.25- or 3.5-MHz transducer) was performed during 35 episodes of transient myocardial ischemia induced by ergonovine in patients with vasospastic angina (n = 9), by dipyridamole in patients with angiographically assessed coronary artery disease (n = 11) and by balloon occlusion during coronary angioplasty (n = 15). Quantitative texture analysis of gray levels was performed off-line on digitized images during rest conditions, ischemia and the recovery phase in regions showing normal contraction at rest, obvious dyssynergy during ischemia and normal contraction in the recovery phase. In each condition, a control region with normal contraction throughout the study was also evaluated. RESULTS: Chest pain occurred in 23 of the 35 episodes; electrocardiographic (ECG) changes were present in 26 episodes, and consisted of ST segment elevation in 13, ST segment depression in 10 and pseudonormalization of a basally negative T wave in 3. The duration of ischemic episodes was 67 +/- 53 s by symptomatic criteria and 91 +/- 52 s by ECG criteria. The risk region showed an increased end-diastolic mean gray level amplitude in a.u. (arbitrary units) during ischemia (57 +/- 19) compared with rest (38 +/- 15) and recovery (38 +/- 18, p < 0.01). No significant changes were detected in the control region (rest 36 +/- 16 vs. ischemia 34 +/- 18 vs. recovery 31 +/- 13, p = NS). The percent increase in mean gray level was similar in the various types of stress employed (ergonovine, dipyridamole or angioplasty) and was not significantly correlated with either the duration of ST segment shift (r = 0.05, p = NS) or the severity of dyssynergy evaluated semiquantitatively by means of the wall motion score (r = 0.28, p = NS). In the 15 balloon occlusions performed in six patients during coronary angioplasty, the increased echoreflectivity of the risk zone was already evident during echocardiographic sampling performed after 10 +/- 4 s of occlusion (rest 35 +/- 9 vs. 53 +/- 10 a.u., p < 0.01) when no dyssynergy could be detected by quantitative wall motion analysis (percent area change by fixed center of mass reference system 31 +/- 10% at rest vs. 32 +/- 11% after 10 s of occlusion, p = NS). CONCLUSIONS: Transient short-lasting myocardial ischemia is associated with an abrupt increase in myocardial echodensity detectable by videodensitometric analysis applied to standard transthoracic echocardiographic images and is largely independent of the underlying pathogenetic mechanism (reduced blood supply or flow maldistribution with coronary stenosis). During controlled coronary occlusion, increased echodensity precedes the onset of regional dyssynergy.

Analysis of Variance↗
PubMed1995

Enhanced insulin response relates to acetylcholine-induced vasoconstriction in vasospastic angina.

OBJECTIVES: This study investigated whether insulin response to an oral glucose load correlates to acetylcholine-induced coronary vasoconstriction in subjects with vasospastic angina. BACKGROUND: It has been suggested that coronary vasospasm is caused by augmented vascular responsiveness possibly exerted by atherosclerosis. Recently, insulin resistance syndrome has been proposed as a major promotor of atherosclerotic disease, potentially enhancing vascular smooth muscular tone. METHODS: Among subjects with angiographically smooth coronary arteries, we selected 14 subjects with vasospastic angina and 14 age- and gender-matched subjects with atypical chest pain. We compared coronary vasomotor response to acetylcholine infusion, glucose and insulin responses to an oral glucose load (75 g), serum lipid concentrations, obesity, heart rate, blood pressure and smoking habits in both groups. RESULTS: Fasting serum insulin concentrations and insulin response were higher in subjects with vasospastic angina than in those with atypical chest pain; however, glucose tolerance, obesity, heart rate, blood pressure and smoking habits did not differ between groups. In subjects with vasospastic angina, nearly all coronary segments, except distal segments of the left circumflex coronary artery, were constricted at peak acetylcholine infusion (20 to 100 micrograms), whereas all segments were dilated in subjects with atypical chest pain. Regression analysis for both groups demonstrated a correlation between coronary vasoconstriction and fasting serum insulin concentrations (r = 0.52, p < 0.01), insulin response (r = 0.71, p < 0.001), serum triglyceride concentrations (r = 0.51, p < 0.05) and atherogenic index (r = 0.44, p < 0.05). CONCLUSIONS: Results show that acetylcholine-induced coronary vasoconstriction in subjects with vasospastic angina correlates with hyperinsulinemia and enhanced insulin response, suggesting insulin resistance syndrome as a feature of vasospastic angina.

Acetylcholine↗
PubMed1986

Coronary artery spasm. Part 1: Overview.

The syndrome of coronary artery spasm is described. This phenomenon may occur in conjunction with, or in the absence of, fixed atherosclerotic coronary artery disease. ECG manifestations during an attack mimic those seen with acute myocardial injury, but normalization of the ECG following the resolution of the pain is usual. Intravenous ergonovine is a sensitive and specific test for confirmation of the diagnosis. Nitrates and calcium channel blockers are the mainstay of therapy, although other agents are of theoretical benefit. The role of surgery is unclear.

Angina Pectoris, Variant↗
PubMed2006

Common adrenergic receptor polymorphisms as novel risk factors for vasospastic angina.

BACKGROUND: Sympathetic activity mediated by adrenergic receptors (ARs) appears to play an important role in controlling the vasomotor tone and, thus, may be associated with vasospastic angina (VA). We investigated the association of the common functional polymorphisms of the AR gene and VA. The candidates were alpha2CDel322-325, beta1Gly389Arg, beta2Arg16Gly, and beta2Gln27Glu polymorphisms. METHODS: Eighty-two patients with VA, confirmed by coronary angiography with or without ergonovine provocation test, and 114 apparently healthy control subjects were investigated for genotype of 4 AR polymorphisms and established risk factors of ischemic heart disease. RESULTS: The minor alleles were alpha2CDel322-325, beta1Gly389, beta2Gly16, and beta2Glu27 and their frequencies were 7%, 18%, 42%, and 29%, respectively, in the control subjects of this Korean population, which were different from those of other ethnic groups. On univariate analysis, age, smoking, male sex, alpha2CDel322-325 allele carrier state, and beta2Gln27 homozygote state were significant risk factors for VA. After multivariate analysis using multiple logistic regression model, age (odds ratio [OR] 1.809, CI 1.046-1.135, P < .0001), smoking (OR 4.902, CI 2.105-11.416, P = .0002), alpha2CDel322-325 allele carrier state (OR 5.132, CI 2.094-12.578, P = .0003), and beta2Gln27 allele homozygosity (OR 3.152, CI 1.364-7.285, P = .0072) remained as independent risk factors. In the combined genotype analysis, the effect of beta2Gln27 allele was evident only when the alpha2CDel322-325 allele was absent. CONCLUSIONS: The alpha2CDel322-325 allele carrier state and beta2Gln27 allele homozygote state were identified as novel risk factors of VA in this Korean population. This result suggests the importance of the adrenergic stimuli and the genetic background in the pathogenesis of the VA.

Adult↗
PubMed2005

Relation of high-sensitivity C-reactive protein level with coronary vasospastic angina pectoris in patients without hemodynamically significant coronary artery disease.

We prospectively investigated the relation of high-sensitivity C-reactive protein (hs-CRP) to coronary vasospasm and no hemodynamically significant coronary artery disease (CAD) in a sample of 428 patients who underwent coronary angiography. These patients were assigned to 1 of 3 groups. The control group consisted of 66 patients who had no coronary vasospasm and no hemodynamically significant CAD. The vasospasm group consisted of 116 patients who had coronary vasospasm and no hemodynamically significant CAD. The acute coronary syndrome (ACS) group consisted of 246 patients who had ACS and hemodynamically significant CAD. Serum hs-CRP was measured immediately before coronary angiography. Patients were followed for subsequent cardiac events and mortality. Median hs-CRP levels in the control, vasospasm, and ACS groups were 1.0, 5.5, and 8.2 mg/L, respectively. The proportion of hs-CRP increased from the lowest to the highest tertile in the control, vasospasm, and ACS groups, respectively. In the control and vasospasm groups, multivariate analysis showed that hs-CRP was independently associated with a diagnosis of coronary vasospastic angina pectoris (odds ratio 68.74, 95% confidence interval 8.03 to 588.71, p<0.001). During a median follow-up period of 26 months (range 0.4 to 48), 27 cardiac deaths occurred in the ACS group, whereas no cardiac death occurred in the control and vasospasm groups. In conclusion, serum hs-CRP level measured immediately before coronary angiography was an independent marker of coronary vasospasm in patients who had no hemodynamically significant CAD.

Aged↗
PubMed2006

High serum matrix metalloproteinase-9 level predict increased risk of in-hospital cardiac events in patients with type 2 diabetes and ST segment elevation myocardial infarction.

INTRODUCTION: The purpose of this study was to compare serum matrix metalloproteinase (MMP)-9 levels in a population of type 2 diabetic versus non-diabetic patients hospitalized with ST-segment elevation myocardial infarction (STEMI) and to examine the relationship between serum MMP-9 levels and the incidence of in-hospital cardiac events, including death and cardiogenic shock. METHODS: We recruited 120 patients with STEMI, of whom 48 were type 2 diabetic and 72 non-diabetic. Serum MMP-9 levels were measured on admission, using a commercially available ELISA. The primary study endpoint was cardiac death in-hospital and cardiogenic shock. RESULTS: Mean serum MMP-9 levels were significantly higher in type 2 diabetic patients compared to non-diabetic patients (240+/-52 ng/mL versus 185+/-47 ng/mL; P<0.0001). In multivariable analysis, type 2 diabetes was an independent factor for mortality [OR: 1.75 (1.40-2.30); P=0.005] and cardiogenic shock [OR: 1.55 (1.20-1.70); P=0.03] when the variable MMP-9 level was not introduced into the model, but it was less significantly associated with mortality [OR: 1.60 (1.40-2.10); P=0.01] and no longer associated with cardiogenic shock when MMP-9 was in the model. CONCLUSION: After STEMI, type 2 diabetes is independently associated with high serum MMP-9 levels. This elevated MMP-9 is strongly associated with the increased incidence of in-hospital mortality and cardiogenic shock observed in type 2 diabetes. Our findings clearly indicate that serum MMP-9 provides a highly valuable prognostic information on in-hospital outcome after STEMI, in particular in type 2 diabetic patients.

Aged↗