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PubMed2006

Klotho gene polymorphism may be a genetic risk factor for atherosclerotic coronary artery disease but not for vasospastic angina in Japanese.

BACKGROUND: The klotho gene, originally identified by insertional mutagenesis in mice, suppresses multiple aging phenotypes, including atherosclerosis. We tested the hypothesis that the G-395A polymorphism of the klotho gene is associated with increased risk for 2 types of ischemic heart disease in Japanese. METHODS: The study population consisted of 197 patients with coronary heart disease (CAD) who had >75% luminal diameter narrowing, 77 patients with vasospastic angina (VSA) without significant fixed coronary artery disease, and 331 healthy control subjects. RESULTS: The frequency of the A allele carriers of the klotho gene was significantly higher in the CAD group than in the control group (29.9% vs. 19.0%). The unadjusted odds ratio for CAD in the A allele carriers compared with the control group was 1.82 (p=0.004) and a traditional risk-adjusted logistic regression model revealed that the A allele was an independent predictor of CAD (odds ratio, 1.76; p=0.03). In contrast, the frequency of the A allele carriers was not significantly different in the VSA group (23.4%; adjusted odds ratio, 1.18. CONCLUSIONS: The -395A polymorphism of the human klotho gene may be a genetic risk factor for IHD and not for VSA.

Adult↗
PubMed2004

Transient giant R-wave, right axis deviation, and intraventricular conduction delay during exercise treadmill testing: a case report.

A 53 year old man complained of chest pain during an exercise treadmill test. Electrocardiogram revealed transient giant R-wave, right-axis deviation, intraventricular conduction delay, and ST-segment elevation in the inferolateral leads. Subsequent coronary angiography showed an 80% lesion in mid part of a nondominant left circumflex artery, whereas the other coronary arteries had mild atherosclerosis only. Percutaneous coronary intervention and stenting was performed on the left circumflex artery lesion. A follow-up exercise thallium scan 3 months later still showed an intermediate-sized, mild reversible perfusion defect in the inferior and lateral wall but the giant R-wave ECG pattern was not inducible anymore. Restudy coronary angiography showed no in-stent restenosis, but there was disease progression in the midpart of the right coronary artery. The initial electrocardiographic pattern is typical of the "giant R-wave syndrome." Severe coronary spasm superimposed on the underlying mild atherosclerotic lesion of the right coronary artery is hypothesized to be the cause of the initial event. Ad hoc direct stenting was performed on the right coronary artery lesion. The patient remained symptom-free with a normal thallium scan 9 months later.

Angina Pectoris, Variant↗
PubMed2005

Structural and functional abnormality of systemic microvessels in cardiac syndrome X.

BACKGROUND AND AIM: Microvascular damage of coronary bed has been considered the main pathogenetic factor of cardiac syndrome X (chest pain, exercise-induced ischemic ST-segment changes and angiographically normal coronary arteries). Previous studies have demonstrated that vascular abnormalities are not confined to the heart, suggesting a peripheral vascular dysfunction. On the hypothesis of a generalized microvascular disturbance in cardiac syndrome X, we performed a morphologic and functional study of systemic microcirculation in patients with syndrome X compared to normal subjects. METHODS AND RESULTS: Microvessels were evaluated with intravital videocapillaroscopy (VCP) executed in peripheral and conjunctival observation sites which explore micro and paramicrocirculation; biohumoral study included markers of inflammation and of endothelial function, coagulative-fibrinolytic system and lipid metabolism. Videocapillaroscopy showed several morphologic changes (present in high percent of patients with syndrome X and not in controls) and significant quantitative alterations (capillary density, granular flow score, alterations of vessel profile, length of capillary loop branches and of arteriole/venule diameter) which indicated a severe alteration of whole vessel structure and an important rearrangement of microvascular disposition. In a similar way, the humoral study showed some significant changes of endothelial (vWF, ICAM-1, E-sel, PAI-1), inflammatory (C-reactive protein (CRP), fibrinogen) and metabolic factors (HDL-chol) which are commonly associated with inflammatory response. CONCLUSIONS: We conclude that patients with cardiac syndrome X exhibited some structural and functional alterations of systemic microvasculature; the pattern is similar to that detected in systemic inflammatory diseases and suggests a vascular lesion of inflammatory type. The same changes could be operating also in coronary microvessels of patients with syndrome X.

Angina Pectoris↗
PubMed2005

Roles of KATP channels as metabolic sensors in acute metabolic changes.

Physiological and pathophysiological roles of K(ATP) channels have been clarified recently in genetically engineered mice. The Kir6.2-containing K(ATP) channels in pancreatic ss-cells and the hypothalamus are essential in the regulation of glucose-induced insulin secretion and hypoglycemia-induced glucagon secretion, respectively, and are involved in glucose uptake in skeletal muscles, thus playing a key role in the maintenance of glucose homeostasis. Disruption of Kir6.1-containing K(ATP) channels in mice leads to spontaneous vascular spasm mimicking vasospastic (Prinzmetal) angina in humans, indicating that the Kir6.1-containing K(ATP) channels in vascular smooth muscles participate in the regulation of vascular tonus, especially in coronary arteries. Together with protective roles of K(ATP) channels against cardiac ischemia and hypoxia-induced seizure propagation, it is now clear that K(ATP) channels, as metabolic sensors, are critical in the maintenance of homeostasis against acute metabolic changes.

ATP-Binding Cassette Transporters↗
PubMed1990

Exercise-induced silent myocardial ischemia in patients with vasospastic angina.

UNLABELLED: To clarify the incidence and clinical characteristics of exercise-induced myocardial ischemia in patients with vasospastic angina, we performed exercise thallium computed tomography in 25 patients who had no significant coronary artery stenosis greater than 70%. Coronary artery spasm was documented by coronary angiography in all patients. Eleven patients (44%) developed exercise-induced perfusion defects, but only four of them had anginal pain (36%). Diltiazem (90 mg, administered orally) prevented the development of exercise-induced perfusion defects in all patients. Multivessel coronary spasm was documented by coronary angiography in 11 patients, and nine of them (82%) showed exercise-induced perfusion defects (p less than 0.05). CONCLUSION: (1) Exercise-induced myocardial ischemia was demonstrated in 44% of patients who had vasospastic angina without fixed coronary stenosis, and 64% of them were asymptomatic. (2) Patients with multivessel spasm had a greater prevalence of exercise-induced myocardial ischemia than those with single-vessel spasm.

Angina Pectoris, Variant↗
PubMed1981

Improved interpretation of a continuous variable in diagnostic testing: probabilistic analysis of scintigraphic rest and exercise left ventricular ejection fractions for coronary disease detection.

The interpretation of a diagnostic modality requires consideration of the entire distribution of potential responses in both the normal and diseases population to extract the maximum available information from the test. Accordingly, we developed a probabilistic format for interpretation of scintigraphic left ventricular ejection fraction (LVEF) in the diagnosis of coronary artery disease (CAD). This format is distinguished (1) by accurate assessment of CAD likelihood based upon age, sex, and symptom classification using a logistical regression model (mean r = 0.9991, mean SEE = 0.008) and (2) by consideration of LVEF as a continuous probabilistic variable which obeys beta frequency distribution. This format allows assessment of the probability of CAD in an individual patient, according to Bayes' theorem of conditional probability of disease, given combinations of LVEF at rest and/or with exercise, and thereby is designed to provide more information than conventional categorical classification of "normal" or "abnormal" test observations.

Adult↗
PubMed1997

Assessment of regional sympathetic nerve activity in vasospastic angina: analysis of iodine 123-labeled metaiodobenzylguanidine scintigraphy.

With the use of iodine 123-labeled metaiodobenzylguanidine (123I-MIBG) scintigraphy, this study evaluated regional sympathetic nerve activity in vasospastic angina. Twenty male patients with left anterior descending coronary artery spasm and 18 male patients with normal coronary arteries as a control group were studied. All patients underwent quantitative 123I-MIBG scintigraphy and atropine stress 123I-MIBG scintigraphy. Both groups showed a similar heterogeneous 123I-MIBG uptake in the left ventricle. However, the regional washout rate in patients with coronary artery spasm was significantly reduced in all three territories compared with that in the control group. In vasospastic angina, the regional washout rate in the left anterior descending coronary artery territory was significantly reduced as compared with the other two regions. After intravenous injection of 1 mg atropine, the regional washout rate in the three regions significantly increased in both groups, but the regional differences between the two groups disappeared. The current study demonstrated that cardiac sympathetic nerve activity in vasospastic angina was suppressed, especially in the territory of the spasm-induced coronary artery, probably because of the enhanced parasympathetic nerve activity.

3-Iodobenzylguanidine↗
PubMed1977

Cardiac prostaglandin release during myocardial ischemia induced by atrial pacing in patients with coronary artery disease.

The relation between myocardial release of prostaglandin and myocardial ischemia was studied in 12 selected patients with multivessel coronary artery disease. These 12 were chosen for analysis because they experienced angina pectoris, ischemic electrocardiographic changes and decreased myocardial lactate uptake during atrial pacing. Simultaneous aortic and coronary sinus blood samples were obtained at rest, during angina and after recovery and were assayed for prostaglandins F, E and A with radioimmunoassay. Cardiac release of prostaglandin F was observed during angina in 11 of 12 patients. Aortic prostaglandin levels remained constant throught each study. During angina, the mean aortovenous difference (+/- standard error) was -0.30 +/- 0.04 ng/ml (P less than 0.001) for prostaglandin F and -0.10 +/- 0.03 ng/ml (Pless than 0.001) for prostaglandin E. There was no significant release of prostaglandin A. Blood samples were also drawn at subanginal heart rates in two patients. Prostaglandin F was released only during angina. In three control patients with a chest pain syndrome and normal coronary arteries, comparable atrial pacing produced no release of prostaglandin F, E or A. These results, together with the known vascular and metabolic actions of prostaglandins, suggest that these pharmacologically active compounds may also play a physiologic role in the cardiac response to ischemia in man.

Adult↗
PubMed1982

Diltiazem for long-term therapy of coronary arterial spasm.

The first 36 patients with coronary arterial spasm treated with diltiazem and followed up at the Stanford University Coronary Artery Spasm Clinic for 6 months or longer are described. There were 13 men and 23 women with a mean age of 50.2 years; the mean duration of angina was 36.1 months. All patients had angina at rest with a good or fail response to sublingual nitroglycerin. During a mean of 17.5 months of diltiazem therapy, the frequency of angina was reduced from a mean of 21.5 to 1.3 attacks/week. This 94 percent reduction in pain frequency occurred when either 240 or 360 mg of diltiazem was administered daily. Sixteen patients required the addition of isosorbide dinitrate to achieve a painfree state. Pain breakthrough occurred a mean of 1.7 times during the 17.5 month follow-up period but tended to be of short duration. Six patients had trace to 1+ pedal edema and no other adverse effects occurred. It is concluded that diltiazem is highly effective and well tolerated for the long-term prophylaxis and treatment of angina in patients with coronary spasm.

Adult↗
PubMed1983

Intravenous nitroglycerin for the treatment of angina at rest unresponsive to standard nitrate therapy.

Thirty-five patients who had angina at rest that was unresponsive to standard therapy comprised of oral or topical nitrates and beta-blocking drugs were treated with a continuous infusion of intravenous nitroglycerin (IVNTG). The infusion was started at 10 micrograms/min and increased by 10 micrograms/min increments every 5 minutes until an infusion rate of 50 micrograms/min was reached. After each episode of rest angina, the infusion was increased by 50 micrograms/min in the same stepwise manner. Data from a 24-hour baseline control period were compared with those from a 24-hour IVNTG endpoint period at which time the highest IVNTG infusion rate was administered. The average IVNTG infusion rate was 140 +/- 15 micrograms/min. With IVNTG therapy, the number of episodes of angina at rest decreased from 3.5 +/- 0.4 to 0.3 +/- 0.1, sublingual nitroglycerin use decreased from 1.9 +/- 0.3 to 0.4 +/- 0.1 mg/day, and morphine sulfate administration decreased from 5.5 +/- 1.3 to 0.4 +/- 0.2 mg/day (all p less than 0.001). When each patient's response on the endpoint day was analyzed, 25 were defined as complete (no rest angina), 8 as partial (greater than 50% decrease in the number of episodes/day from control values), and 2 as nonresponders. No significant drug-induced adverse effects occurred. IVNTG appears to be effective therapy for angina at rest refractory to standard oral and topical medications.

Adult↗
PubMed1997

Comparison of coronary flow reserve between focal and diffuse vasoconstriction induced by ergonovine in patients with vasospastic angina.

Decreased coronary flow reserve has been reported in patients with ergonovine-induced coronary vasoconstriction by the thermodilution method. To assess the difference of coronary flow reserve between patients with focal and diffuse vasospasm, after the vasospasm is discontinued by injection 3 mg of isosorbide dinitrate, phasic flow velocities of the diseased coronary artery were recorded at rest and during hyperemia (140 microg/kg/min of adenosine infusion intravenously) using a 0.014-inch, 15-MHz Doppler guidewire in 26 patients with ergonovine-induced coronary vasospasm (0.2-mg ergonovine injection intravenously), including 12 patients with focal (>90% stenosis), 14 patients with diffuse vasospasm (>50%), and 11 controls with normal coronary arteries without vasospasm. Although time-averaged peak velocity in cases with diffuse and focal vasospasm was not significantly different compared with that in controls at baseline (22 +/- 7, 18 +/- 5 vs 20 +/- 7 cm/s, respectively, NS), it was significantly lower in patients with diffuse vasospasm than in cases with focal vasospasm and in controls during hyperemia (43 +/- 13 vs 64 +/- 18, 61 +/- 19 cm/s, respectively, p <0.01). As a result, coronary flow reserve obtained from the ratio of hyperemic/baseline time-averaged peak velocity was significantly lower in patients with diffuse vasospasm than that in controls (1.9 +/- 0.4 vs 3.1 +/- 0.4, p <0.01), although it was not significantly different between the subjects with focal vasospasm and controls (3.5 +/- 0.7 vs 3.1 +/- 0.4, NS). Thus, coronary flow reserve is maintained normally in patients with focal vasospasm and limited in those with diffuse vasospasm. Microvascular impairment could exist further in cases with diffuse vasospasm, although similar endothelial dysfunction of the epicardial coronary artery is observed in focal and diffuse vasospasm.

Adult↗
PubMed1998

Effect of diltiazem on sympathetic hyperactivity in patients with vasospastic angina as assessed by spectral analysis of arterial pressure and heart rate variability.

The autonomic nervous system importantly regulates coronary arterial tone and vascular resistance. To evaluate a role of autonomic nervous activity and the effects of calcium antagonist in patients with vasospastic angina (VSA), 13 VSA patients with patent coronary arteries (58+/-8 years) and 8 normal subjects (58+/-12 years) were studied. Arterial pressure and electrocardiogram were continuously recorded with the patient in a supine position under controlled respiration (0.2 Hz). Low-frequency (LF) and high-frequency (HF) components of the beat-to-beat variabilities of systolic arterial pressure and RR interval were then estimated by autoregressive power spectral analysis. The LF power (normalized unit) of both systolic arterial pressure (0.53+/-0.17 vs 0.30+/-0.17, p < 0.01) and RR variabilities (0.51+/-0.20 vs 0.31+/-0.16, p < 0.05) in patients with VSA were greater than that in normal subjects. There was no significant difference in the HF power. Seven patients with VSA who were treated with diltiazem (60 to 200 mg/day) had normalized LF power (normalized unit) of both systolic arterial pressure (0.62+/-0.12 vs 0.33+/-0.16, p < 0.01) and RR variabilities (0.55+/-0.23 vs 0.36+/-0.14, p < 0.05), together with clinical improvement. An increased sympathetic vasomotor tone and cardiac sympathetic predominance may play an important role in patients with VSA. Diltiazem improves these sympathetic hyperactivities.

Angina Pectoris, Variant↗
PubMed1996

Induction of polymorphic ventricular tachycardia by programmed ventricular stimulation in vasospastic angina pectoris.

This study was designed to examine the ventricular vulnerability of patients with vasospastic angina. Fourteen patients (mean age 57 +/- 9 years) with vasospastic angina underwent electrophysiologic testing during the asymptomatic phase (baseline) and after the relief of acetylcholine-induced spasm with isosorbide dinitrates. Twenty patients without structural heart disease served as a control group. By programmed ventricular stimulation, polymorphic ventricular tachycardia (VT) was induced at baseline in 6 of 14 patients, with 1 patient developing ventricular fibrillation and 7 of 14 patients developing repetitive ventricular responses. After isosorbide dinitrate, polymorphic VT was induced in only 1 patient who had ventricular fibrillation at baseline. Repetitive ventricular responses were induced in 3 of 5 patients who had VT at baseline and in 4 of the 7 patients with repetitive ventricular responses at baseline. There was a significant difference in the incidences and severity of induced ventricular arrhythmias between the 2 phases (p <0.01). Among 20 control subjects, repetitive ventricular responses were induced only in 6 patients, but no VT was induced. There was a significant difference in the incidence of induced ventricular arrhythmias and VT at baseline between the vasospastic angina and control groups (p <0.001 and <0.01, respectively). Thus, patients with vasospastic angina had increased ventricular vulnerability, even during the symptom-free period without ischemic events, which could predispose to the development of life-threatening arrhythmias aggravated by vasospastic attacks.

Adult↗
PubMed1999

Relation between the electrocardiographic stress test and degree and location of myocardial ischemia.

Factors that influence frequency and location of stress-induced electrocardiographic (ECG) ST depression and the development of chest pain are incompletely understood. We studied 331 patients with ischemic myocardial nuclear defects in response to routine clinical treadmill testing with simultaneous ECG recording. Nuclear defects were analyzed for location and extent of myocardium involved. Exercise-induced ischemic ST changes were demonstrated in 59% of patients (196 of 331). Subjects with stress-induced ECG changes and/or chest pain had more extensive nuclear perfusion defects. Diabetic patients were significantly less likely to experience chest pain (24%) versus nondiabetics (41%) during testing (p = 0.04). Larger perfusion defects were associated with greater magnitude, lead distribution, and incidence of ECG changes. The number of ECG lead zones (anterior, lateral, and inferior) responding positively were related to both magnitude of ST depression and severity of ischemia, but not to location of ischemic defects. Regardless of location of ischemia, ST depression occurred with similar frequency. Thus, exercise-induced ECG ST depression remains a valuable indicator of the severity of myocardial ischemia. Greater ST depression involving multiple leads usually signified extensive myocardial ischemia, but provided no information regarding its location. Anginal-type chest pain induced by exercise testing also denoted more extensive ischemia.

Adult↗