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At least 19 recordsLinked to original sources
PubMed1992

Cutaneous and coronary flow reserve in patients with microvascular angina.

Microvascular angina is characterized by exercise-induced angina in patients with normal coronary arteries and reduced coronary flow reserve. Recently, a generalized disorder of abnormal vascular reactivity in microvascular angina has been postulated. Therefore, coronary flow reserve was determined by the coronary sinus thermodilution technique and compared with the cutaneous flux ratio in 6 control subjects (group 1) and 12 patients with microvascular angina (group 2). Coronary flow reserve was calculated from maximal coronary flow after 0.5 mg/kg of dipyridamole divided by flow at rest. Cutaneous flow ratio was estimated by laser Doppler fluxmetry (right forearm) before and after 4 min of suprasystolic blood pressure occlusion. Coronary flow at rest was identical in the two groups, but after maximal vasodilation with dipyridamole, coronary flow was higher in group 1 than in group 2 (p less than 0.05). Coronary flow reserve differed significantly between the two groups (2.9 in group 1 and 1.3 in group 2; p less than 0.001). Cutaneous Doppler flux at rest was higher in group 1 than in group 2 (p less than 0.05). However, the hyperemic response was identical in both groups. It is concluded that the cutaneous flux ratio in patients with microvascular angina is not impaired. Local peripheral vasomotor tone appears to be increased in patients with microvascular angina because cutaneous flow at rest is reduced. Thus, a generalized disorder of abnormal vascular reactivity cannot be confirmed in patients with microvascular angina.

Adult↗
PubMed1995

Effect of diltiazem on coronary flow reserve in patients with microvascular angina.

Microvascular angina is characterized by ischemia-like symptoms in patients with normal coronary arteries and reduced coronary flow reserve. Clinical observations suggested an improvement in clinical symptomatology and exercise tolerance after treatment with calcium antagonists. The effect of diltiazem on coronary flow reserve was evaluated in controls and in patients with microvascular angina. Coronary flow reserve was measured in 16 normotensive patients (7 females, 9 males, mean age 51 +/- 10 years) with angiographically normal coronary arteries. Coronary blood flow was determined at rest, after dipyridamole (0.5 mg/kg) and following intravenous administration of diltiazem (10 mg) using coronary sinus thermodilution technique. Coronary flow reserve was calculated as coronary blood flow after dipyridamole divided by coronary blood flow at rest. Patients with normal coronary flow reserve (coronary flow reserve > 2.0) received either dipyridamole alone (group 1, controls, n = 6) or dipyridamole and diltiazem (group 2, n = 5), whereas patients with reduced coronary flow reserve (coronary flow reserve < 2.0) obtained dipyridamole and diltiazem (group 3, n = 5). Resting coronary flow was identical in the three groups, but after maximal vasodilation with dipyridamole, coronary flow increased significantly more in groups 1 and 2 than in group 3 (P < 0.05, analysis of variance (ANOVA)). Coronary flow reserve was 2.5 in group 1 and 2.3 in group 2, but was significantly reduced in group 3 (1.3; P < 0.05, ANOVA). Intravenous diltiazem failed to increase coronary blood flow in groups 2 and 3. Therefore, diltiazem does not improve reduced coronary flow reserve in patients with microvascular angina, but leaves coronary flow reserve unaffected. The failure to ameliorate impaired coronary flow reserve with diltiazem is in contrast to the reported clinical improvement after calcium channel blockade in these patients. Thus, other factors such as structural abnormalities in the microcirculation or functional abnormality in smooth muscle relaxation not responsive to calcium channel blockade are probably responsible for the occurrence of myocardial ischemia in patients with microvascular angina.

Analysis of Variance↗
PubMed2001

Recent developments in microvascular angina.

Microvascular angina (Syndrome X) is an extremely heterogeneous clinical entity that is the product of genetic, coronary microvascular, metabolic, and clinical factors, which combine together to produce distinct cardiac manifestations and complications. The interactions of these abnormalities remain poorly understood. The diagnosis is considered in patients with anginal symptoms and no epicardial coronary narrowing. Therapy is also problematic, with beta-blockers as first-line pharmacotherapy followed by angiotensin-converting enzyme inhibitors and calcium channel blockers.

Adrenergic beta-Antagonists↗
PubMed1996

Changes in myocardial lactate metabolism during ramp exercise in patients with effort angina and microvascular angina.

Changes in myocardial lactate metabolism during ramp exercise were investigated through great cardiac vein catheterization in 15 patients with effort angina (EA) and 7 patients with microvascular angina (MVA). The exercise test was performed using a supine bicycle ergometer. Blood samples were obtained from the great cardiac vein (GCV) and the radial artery each minute during exercise. Patients in the EA group showed a point at which the lactate extraction ratio (LER) and the ST level decreased rapidly during exercise. This point was clearly recognized in 12 of 13 patients, and may represent the ischemic threshold. Both the LER and ST level showed similar changes during exercise, and these values were significantly different between the ischemic threshold and peak exercise (p < 0.01). Both the LER and ST level were strongly correlated with the duration of exercise until the threshold (r = 0.703). In the MVA group, both the LER and ST level during exercise continuously decreased throughout exercise without an ischemic threshold in all of the subjects. Endomyocardial biopsy revealed sclerosis of small arteries in the myocardium in all of the patients. In both effort angina and microvascular angina, a close correlation was noted between the change in ST and that in the myocardial lactate extraction ratio.

Adult↗
PubMedDate not supplied

[The dipyridamole-echo-ECG test in hypertensives with microvascular angina].

Microvascular angina - chest pain syndrome in the presence of angiographically normal epicardial coronary arteries and reduced flow reserve - has been also described in patients with essential hypertension and it has been linked to the development of left ventricular hypertrophy. Dipyridamole-Echocardiography Test (DET: 2D-echo and 12 lead ECG monitoring with dipyridamole infusion, up to 0.84 mg/kg over 10') was performed in 28 essential hypertensives meeting the following inclusion criteria; 1) history of chest pain; 2) angiographically normal coronary arteries; 3) normal resting regional and global left ventricular function. A group of 12 (age and sex matched) normotensives with the same inclusion criteria, as well as with negative exercise stress test, was also evaluated. During DET, none, either in essential hypertensives or in control group, developed a regional dyssynergy of contraction; 15 in essential hypertensives, and 2 in control group had a diagnostic (greater than 0.1 mVolt from baseline) ST segment depression on ECG tracing (54 vs 17% p less than 0.01); 16 in essential hypertensives and 2 in control group had chest pain (57 vs 17%, p less than 0.01). None of the control group and 9 of the essential hypertensives had echocardiographically assessed left ventricular hypertrophy. In the essential hypertensives group, ventricular hypertrophy was present in 7/20 patients with and in 2/8 patients without dipyridamole induced chest pain and/or ST segment depression (35 vs 25%, p = ns). In conclusion, essential hypertensives patients with chest pain and angiographically normal coronary arteries frequently show "echocardiographically silent" angina and/or ST segment depression during DET. The presence of ventricular hypertrophy does not appear to be a prerequisite for the induction of angina in these patients.

Angina Pectoris↗
PubMed2005

Vasospastic angina and microvascular angina are differentially influenced by PON1 A632G polymorphism in the Japanese.

BACKGROUND: Ethnicity and smoking are well-known risk factors for the pathogenesis of coronary vasospasm. Oxidative stress induced by smoking plays a crucial role in coronary vasospasm, but is not enough to account for the pathogenesis of coronary vasospasm, indicating that genetic factors are strongly involved. METHODS AND RESULTS: The study group comprised 162 vasospastic angina patients (VSAs), 61 microvascular angina patients (MVAs) and 61 non-responders (NRs) diagnosed by acetylcholine provocation test. Four polymorphisms of the oxidative stress related genes, cytochrome b-245, alpha polypeptide gene (CYBA) C242T and A640G, paraoxonase 1 gene (PON1) A632G, phospholipase A2 group VII gene (PLA2G7) G994T were genotyped. Allele frequency of PON1 632-G was significantly higher in both the VSA with dominant fashion and the MVA with recessive fashion compared with NR. This association was strongly influenced by gender in the MVA only. There were no significant associations between the other polymorphisms and coronary vasospasm. In addition, the allele frequency of PON1 632-G in the Japanese was higher than in Caucasians. CONCLUSIONS: There was a significant association between PON1 A632G polymorphism and MVA as well as VSA, but the impact of this on VSA and MVA is different in the Japanese.

Acetylcholine↗
PubMed2000

Alteration of coronary flow velocity during spontaneous angina in a patient with microvascular angina.

Phasic coronary flow velocity in the left and right coronary artery was recorded in a patient with microvascular angina. Coronary flow velocity during anginal attack was characterized by diminished systolic forward velocity, the appearance of systolic flow reversal, increase in diastolic flow velocity and its rapid deceleration. It was also accompanied with abnormal coronary flow reserve. These findings completely recovered at follow-up examination. A subgroup of patients with microvascular angina may show unique and reversible coronary flow abnormalities during chest pain.

Aged↗
PubMed2001

Three-year follow-up of the Japanese patients with microvascular angina attributable to coronary microvascular spasm.

BACKGROUND: We recently reported that coronary microvascular spasm could cause angina in patients with chest pain and normal coronary arteriograms. However, the long-term prognosis of these patients or the effect of calcium channel blockers is not known. METHODS: Of consecutive 283 patients who underwent acetylcholine testing for the evaluation of chest pain, we identified 68 patients with microvascular angina attributable to coronary microvascular spasm. All patients were discharged on calcium channel blockers and followed up for an average period of 3.3 years. RESULTS: As compared with those having epicardial spasm (n=169), there was a female predominance in the microvascular spasm group (P<0.01), and 81% of the female patients were postmenopausal. During the follow-up, no patient died and one patient (1%) developed non-Q wave myocardial infarction. The frequency of chest pain was unchanged or increased in 24 patients (36%) and decreased or disappeared in 42 patients (64%). The angina status was improved only in 16 of 33 patients treated with calcium channel blockers alone. By contrast, it was improved in 18 of 21 patients on the combination of calcium channel blockers and angiotensin converting enzyme inhibitors (P<0.05). CONCLUSIONS: Patients with microvascular angina in the present study were more women and had a different risk factor profile as compared with those having epicardial spasm. Long-term prognosis was excellent with regard to mortality, but angina persisted in many patients even on calcium channel blockers. The result warrants prospective studies to evaluate the efficacy of angiotensin converting enzyme inhibitors as adjunct to calcium channel blockers in this population.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Treatment of the hypertensive patient with microvascular angina.

Syndrome X and microvascular angina are a heterogenous group of diseases. Several medications, including angiotensin-converting enzyme inhibitors, beta-blockers, and calcium-channel blockers, have been reported to be successful in the treatment of microvascular angina. Control of hypertension and regression of left ventricular hypertrophy are important in controlling symptoms associated with this intriguing problem. The role of nitric oxide and the effects of L-arginine in the pathogenesis and treatment of hypertension and microvascular angina need to be elucidated. Optimal treatment will depend on the appropriate classification and diagnosis of chest pain in patients with hypertension and normal coronary angiograms.

Adrenergic Antagonists↗
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↗
PubMed1999

The Effect of Trimetazidine in the Treatment of Microvascular Angina.

Although the pathophysiology of microvascular angina is unclear, intracellular metabolic changes are believed to be the main factors. Trimetazidine has an intracellular metabolic effect in coronary insufficiency. The effect of trimetazidine in microvascular angina is unknown. Thirty-five patients (8 men, 27 women, age 36-57 years, mean 43.9 +/- 6.4 years) with microvascular angina were included in this study. The effects of trimetazidine (60 mg daily) were investigated in a placebo-controlled, double-blind study consisting of two 4-week treatment periods. Patients were assessed by symptom-limited exercise testing (Bruce protocol). Heart rate and systolic blood pressure at rest, peak exercise, and the time of 1 mm ST segment depression were not significantly different between placebo and trimetazidine treatment. Trimetazidine prolonged total exercise time and time to 1 mm ST depression compared with placebo. Maximum ST depression was less in patients with trimetazidine therapy than those with placebo. It is concluded that trimetazidine has a beneficial effect in cases with microvascular angina.

Journal Article↗
PubMed1999

Blood pressure profile in patients with microvascular angina.

Normotensive patients with microvascular angina exhibit increased diastolic blood pressure and blood pressure loads during daily activities and decreased diurnal variation of systolic blood pressure, compared with age- and sex-matched normotensive controls. The abnormal blood pressure profile could play a role in the pathogenesis of microvascular angina.

Adult↗
PubMed1993

Insulin resistance in microvascular angina (syndrome X)

Patients with microvascular angina (syndrome X) may be insulin resistant. We designed a study to establish whether this is the case. 11 patients with microvascular angina were compared with 9 matched subjects with noncardiac chest pain. Patients and controls were evaluated by coronary sinus catheterisation, and by isotopic measurement of glucose turnover, indirect calorimetry, and forearm technique during a 3 h baseline period after overnight fast and during a 2 h hyperinsulinaemic euglycaemic clamp. Pace-induced increase in coronary sinus blood flow was less in patients than in controls, whereas forearm blood flow did not differ between groups. Baseline measures of glucose metabolism were normal. During the clamp, glucose production and lipolysis were equally suppressed in both groups. Mean (SE) total insulin-induced glucose uptake was significantly impaired in patients compared with controls (3.9 [0.7] vs 6.4 [0.7] mg/kg per min; p < 0.01), and insulin-stimulated glucose uptake in the forearm was significantly reduced in patients (0.88 [0.10] vs 1.6 [0.30] mmol/L; p < 0.001). Reduced oxidative and nonoxidative metabolism accounted for the defect in overall glucose uptake in patients. No correlation between changes in coronary sinus blood flow and total body glucose uptake was seen. We found that microvascular angina was associated with substantial insulin resistance. Whether this relation is causal or coincidental is as yet unsettled.

Alanine↗
PubMed1994

Breathlessness in microvascular angina.

In patients with microvascular angina (MA), there is some evidence from studies of plethysmography, that there are widespread microvascular abnormalities. In addition to exertional chest pain, all these patients complain of breathlessness, with no evidence of airways obstruction or resting left ventricular dysfunction. Progressive exercise testing was performed in 12 age and sex matched controls and 12 patients (three males), in whom the diagnosis of MA was established on the basis of exertional chest pain, abnormal thallium scans, and an attenuated myocardial flow response to a vasodilator challenge, with angiographically entirely normal epicardial vessels. Symptom limited exercise was performed with on line ventilation and expired gas analysis, measuring minute ventilation, oxygen consumption and carbon dioxide production and arterial blood gas values using a transcutaneous system. Anaerobic threshold was calculated by curve fitting a plot of oxygen consumption against carbon dioxide production. Compared to controls (49.7 +/- 7.3 SD% predicted maximum VO2) in patients with MA, the anaerobic threshold was reduced (41.6 +/- 5.82; P < 0.02) although still within accepted normal limits. Maximal (symptom limited) oxygen consumption, as a percentage of predicted, was reduced 60.73 +/- 16.51 compared to 87.21 +/- 5.2 (P < 0.003). The ventilatory response (VE/VCO2 l l-1 CO2 output) was significantly increased in the MA patients compared to controls (35.9 +/- 8.01 and 27.5 +/- 3.08, respectively; P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Therapy of microvascular angina].

The treatment of microvascular angina (anginal pain resulting from myocardial ischemia due to dysfunction of small coronary arteries) is empiric and often ineffective at present. The poor knowledge of the pathophysiologic mechanisms responsible for the microvascular dysfunction and the possible heterogeneous nature of the disease limit the possibility of a rational therapeutic approach to these patients. The failure of traditional antiischemic therapy is confirmed by the frequent unresponsiveness of angina and by the reduced exercise tolerance with administration of sublingual nitrates. Despite that, beta-blockers and calcium-antagonists, when given either alone or in combination, are beneficial in the control of symptoms in some patients. Alternative forms of treatment, based on some pathophysiological hypotheses and clinical observations, include xanthine derivatives, ACE-inhibitors, alpha-blocking agents, imipramine and, in women, oestrogens. The actual clinical usefulness of these drugs, however, is questionable at present, as their efficacy should be evaluated with more adequate studies in the future.

Adrenergic alpha-Antagonists↗
PubMed1995

Insulin resistance and hyperlipoproteinemia in microvascular angina: risk factors or pathogenetic link?

BACKGROUND: Patients with chest pain and normal epicardial coronary arteries (microvascular angina; syndrome X) are characterized by an impairment of myocardial perfusion reserve which may be related to functional and morphological abnormalities of the intramyocardial arterioles. METHODS: In an attempt to identify predisposing factors for microvascular angina we investigated 34 consecutive patients (15 female, 19 male; mean age 53 +/- 7 years) with microvascular angina but without hypertension or left ventricular hypertrophy. The metabolic profile, including plasma insulin, glucose, cholesterol, low-density lipoprotein cholesterol, triglycerides, very-low-density lipoprotein cholesterol and fibrinogen levels, was determined in each case. Furthermore, insulin and glucose levels were measured after an oral glucose load of 100 g over 3 h. All parameters were compared with those of a control group of 15 healthy subjects matched for age, sex and body mass index. RESULTS: The systolic blood pressure in microvascular angina was 137 +/- 17 mmHg and thus higher than that of healthy controls (124 +/- 11 mmHg); diastolic blood pressure was 85 +/- 7 compared with 78 +/- 9 mmHg in controls. Insulin level was significantly elevated in patients with microvascular angina 90 min (median: 101 versus 54 microU/ml) and 120 min (median: 88 versus 51 microU/ml) after ingestion of 100 g glucose. The fasting glucose level was 98 +/- 12 versus 87 +/- 7 mg/dl in controls. Glucose concentration was also elevated after 30 min (176 +/- 28 versus 148 +/- 32 mg/dl), after 45 min (198 +/- 35 versus 152 +/- 53 mg/dl) and after 60 min (193 +/- 44 versus 145 +/- 54 mg/dl). In microvascular angina, parameters such as total cholesterol (244 +/- 46 versus 199 +/- 29 mg/dl), low-density lipoprotein cholesterol (157 +/- 41 versus 122 +/- 18 mg/dl) and fibrinogen (377 +/- 150 versus 285 +/- 69 mg/dl) were elevated. CONCLUSIONS: The metabolic profile in patients with microvascular angina suggests a pathogenetic role of insulin resistance and hyperlipoproteinemia in the setting of impaired myocardial coronary reserve and in early stages of hypertensive heart disease.

Adult↗
PubMed1996

Lipid profile in patients with microvascular angina.

Lipid, lipoprotein and apolipoprotein levels, as well as the susceptibility of low-density lipoprotein (LDL) to oxidation, were studied in patients with micro-vascular angina in comparison with patients with coronary artery disease (CAD) and normal subjects. Total cholesterol, LDL-cholesterol and apolipoprotein B levels in microvascular angina patients (235 +/- 46 mg dL-1, 135 +/- 33 mg dL-1 and 146 +/- 32 mg dL-1 respectively) were significantly higher than in control subjects (204 +/- 40 mg dL-1, 116 +/- 35 mg dL-1 and 129 +/- 29 mg dL-1 respectively, P < 0.01). These parameters were also significantly higher in CAD patients than in control subjects. By contrast, high-density lipoprotein (HDL)-cholesterol levels in microvascular angina patients were no different from those in control subjects, although both were significantly higher than in the CAD patients (48 +/- 16 mg dL-1 and 45 +/- 12 mg dL-1 compared with 40 +/- 10 mg dL-1, P < 0.01 and P < 0.05 respectively). Similar results were obtained for the apolipoprotein AI levels. Furthermore, the atherogenic risk ratio, LDL-cholesterol/HDL-cholesterol, in microvascular angina patients was significantly lower than in the CAD patients (3.4 +/- 1.2 vs. 4.1 +/- 1.5 respectively, P < 0.01). Median (range) serum lipoprotein (a) [Lp(a)] levels in microvascular angina patients and CAD patients [13 mg dL-1 (0.8-92) and 16 mg dL-1 (0.8-96) respectively] were significantly higher than in control subjects [7 mg-dL-1 (0.8-44)], P < 0.01 and P < 0.005 respectively. Sigmoidal curves and electrophoretic mobility of the Cu(2+)-oxidized LDL in both microvascular angina and CAD patients were not significantly different from those of control subjects. Finally, no significant differences were found between groups in total triglyceride levels or in very low-density lipoprotein (VLDL), LDL and HDL triglyceride levels. Our results show that the microvascular angina patients exhibit lipid abnormalities similar to those observed in CAD patients, with the important exception of the HDL-cholesterol and apolipoprotein AI levels, which are significantly higher in microvascular angina patients. We suggest that the abnormal cholesterol and Lp(a) levels may be involved in the pathophysiology of microvascular angina by affecting endothelial function and endothelium-mediated vasodilator responses, whereas the higher HDL levels may be a factor contributing to the absence of angiographically documented CAD in microvascular angina patients.

Adult↗