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Results for “Microvascular Angina”

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PubMed1997

Effects of short-term treatment of nicorandil on exercise-induced myocardial ischemia and abnormal cardiac autonomic activity in microvascular angina.

The underlying mechanisms of myocardial ischemia in microvascular angina may include endothelial dysfunction, abnormal smooth muscle tone, and abnormal autonomic control of coronary microvasculatures. This randomized, double-blind, placebo-controlled, crossover study was conducted to evaluate the effect of nicorandil (a nitrate-potassium channel opener) therapy on exercise-induced myocardial ischemia and cardiac autonomic activity in 13 patients with microvascular angina. After a 2-week placebo run-in period, patients were randomly assigned to the first 2-week treatment with nicorandil 5 mg tid or placebo, then crossed over to the second 2-week treatment after a 2-week washout period. Treadmill exercise tests and 24-hour ambulatory electrocardiogram monitoring were performed at the end of each treatment phase. The results showed that both time to 1-mm ST depression and total exercise duration were significantly prolonged with nicorandil treatment compared with placebo (p = 0.026 and 0.036, respectively). Maximum exercise ST depression also tended to be less with nicorandil treatment than with placebo (p = 0.083). Compared with 10 healthy control subjects, study patients had significantly reduced heart rate variability in both low- and high-frequency bands while receiving placebo. Nicorandil treatment did not change the altered heart rate variability in either time domain or spectral analysis. Systemic hemodynamics were also unchanged with nicorandil treatment. Thus, 2-week oral nicorandil therapy moderately improved exercise-induced myocardial ischemia without modifying the already altered cardiac autonomic activity, suggesting that nicorandil might have a direct vasodilatory effect on coronary microvasculatures in patients with microvascular angina.

Administration, Oral↗

PubMed1991

Hyperinsulinaemia and microvascular angina ("syndrome X")

Glucose and insulin responses to a glucose load in 11 patients with angina attributed to microvascular coronary dysfunction were compared with those in 11 healthy subjects matched for age, sex, and body mass. Stimulated hyperinsulinaemia was demonstrated in the microvascular angina group. The findings suggest a role for increased concentrations of insulin in coronary microvascular dysfunction.

Adult↗

PubMed2000

Microvascular angina (cardiological syndrome X) per se is not associated with hyperinsulinaemia or insulin resistance.

BACKGROUND: Microvascular angina has been found to be associated with insulin resistance. However, many factors known to affect insulin sensitivity were not excluded in patient selection. We aimed to evaluate whether microvascular angina is per se associated with insulin resistance. MATERIALS AND METHODS: We performed a Frequently Sampled Intravenous Glucose Tolerance Test (0.33 g kg(-1) b.w.) in 10 normal weight and normotensive patients with microvascular angina, with normal glucose tolerance and normal plasma lipids. Ten healthy subjects, comparable for age, sex, body mass index, blood pressure and plasma lipids, were used as control group. RESULTS: Fasting serum glucose (4.49+/-0.2 SEM vs. 4.52+/-0.13 mmol L(-1), P = 0.9), insulin (39.46 +/-3.68 SEM vs. 47.12+/-4.6 pmol L(-1), P = 0.21) and C-peptide (0.56 +/-0.05 SEM vs. 0.53+/-0.05 nmol L(-1), P = 0. 68) values, as well as estimated parameters of insulin secretion and hepatic insulin extraction were similar in the two groups. Insulin sensitivity values (median, range) were also similar in the patients and control subjects (5.76 (3.39-12.30) vs. 7.54 (3.68-13.89. 10(-4) x min(-1)/(microU/mL), P = 0.97). CONCLUSION: Microvascular angina per se is not associated with hyperinsulinaemia or insulin resistance when other confounding factors are excluded in patient selection.

Adult↗

PubMed1995

[Microvascular angina (syndrome X). Presentation of 4 cases].

OBJECTIVE: To revise diagnostic, therapeutic and evolutive specifications of Microvascular Angina. To improve the knowledge about this syndrome among family doctors. DESIGN: Descriptive and transversal study. SETTING: Outpatients belonging to a Primary Care Centre in the metropolitan area of Madrid. PATIENTS AND OTHER PARTICIPANTS: Four patients (2 male and 2 female) aged over 50, diagnosed to have Microvascular Angina. MEASUREMENTS AND MAIN RESULTS: The clinical histories of the patients diagnosed to have Microvascular Angina were used. This syndrome was defined as a typical chest pain starting by an effort, normal electrocardiogram, ischemic ST-segment depression in exercise stress test and angiographically normal coronary arteries. The clinical and electrocardiographic specifications were similar in four cases. A positive exercise stress test and the existence of normal coronary arteries was confirmed in all the patients. All of them were treated with betablokers and/or calcium channel blokers with an effective response in three of them. CONCLUSIONS: It is important to know the existence of Microvascular Angina in Primary Care, first because it is one cause of chest pain and second because it has a good prognosis with few complications in the future.

Adrenergic beta-Antagonists↗

PubMed2002

Clinical characteristics and follow-up in patients with microvascular angina.

Arteriosclerosis of the small arteries is one of the main causes of microvascular angina, and although some reports have shown favorable prognoses, there is progressive reduction in left ventricular function. The present study evaluated the prognosis of microvascular angina in 86 Japanese patients (51 women, 35 men; average age, 59+/-9 years) who had ischemic ST segment depression, normal coronary angiograms and small artery sclerosis confirmed by endomyocardial biopsies. The mean follow-up period was 7.2+/-3.4 years. Questionnaires regarding their symptoms, cardiac medication, and new events were sent to all patients. Eighty-five patients (98.9%) were still alive at the end of the follow-up period. Chest pain remained in 35.3%; the degree of pain was unchanged in 18.8%, and had lessened in 11.8%. None of the patients died of cardiac events or suffered from a myocardial infarction. At the end of the follow-up period, calcium antagonist was used in 63.5% of patients. Seventeen patients (20.0%) were free of antianginal medication. The prognosis of microvascular angina diagnosed by strict criteria was favorable.

Aged↗

PubMed2000

Coronary microangiopathy in type 2 diabetic patients: relation to glycemic control, sex, and microvascular angina rather than to coronary artery disease.

UNLABELLED: Coronary microangiopathy is a major complication in diabetics. However, the presence of independent factors in association with coronary microangiopathy in patients with non-insulin-dependent diabetes mellitus (NIDDM) or the difference in coronary microangiopathy between diabetics with coronary artery disease (CAD) and those with microvascular angina is unclear. METHODS: Nineteen patients with NIDDM and microvascular angina, 18 patients with NIDDM and CAD, and 17 age-matched control subjects were studied. Myocardial segments that were perfused by angiographically normal coronary arteries were studied. The baseline myocardial blood flow (MBF) and the MBF during dipyridamole administration were measured using PET and 13N-ammonia, after which the myocardial flow reserve (MFR) was calculated to assess coronary microangiopathy. RESULTS: The baseline MBF was comparable among NIDDM patients with microvascular angina, NIDDM patients with CAD, and control subjects. However, the MBF during dipyridamole administration was significantly lower in NIDDM patients with microvascular angina (126 +/- 42.7 mL/min/100 g) than that in either NIDDM patients with CAD (210 +/- 70.1 mL/min/100 g; P < 0.01) or control subjects (293 +/- 159 mL/min/100 g; P < 0.01), as was the MFR (NIDDM with microvascular angina, 1.90 +/- 0.73; NIDDM with CAD, 2.59 +/- 0.81 [P < 0.01]; control subjects, 3.69 +/- 1.09 [P < 0.01]). Multivariate stepwise regression analysis showed that, among the factors considered, glycemic control was independently related to the MFR (r = 0.838; P < 0.05). CONCLUSION: Glycemic control appears to be essential for coronary microangiopathy in NIDDM.

Adult↗

PubMed1990

Airway hyperresponsiveness in patients with microvascular angina. Evidence for a diffuse disorder of smooth muscle responsiveness.

Anginal chest pain in patients with angiographically normal coronary arteries may be caused by a limited coronary flow response to stress because of abnormal function of the coronary microcirculation (microvascular angina). Studies of forearm arterial function suggested that patients with microvascular angina may have a diffuse disorder of smooth muscle tone. Because dyspnea is common in these patients and seems disproportionate to the severity of myocardial ischemia, we studied air flow (forced expiratory volume in 1 second, or FEV1) in the basal state and after methacholine inhalation to determine whether bronchial smooth muscle is affected in this syndrome. Five of 36 patients with microvascular angina had a basal FEV1 of less than 70% of that predicted and did not receive methacholine. Of the remaining 31 patients, 14 (45%) had a more-than-20% reduction in FEV1 after methacholine inhalation (as much as 25 mg/ml), a response significantly greater than that of nine patients with heart disease (0%, p less than 0.025) and 24 normal volunteers of similar age and gender distribution (13%, p less than 0.025). Furthermore, the product of the methacholine dose inhaled and the magnitude of decline in FEV1 from baseline (methacholine response score) was significantly lower in patients with microvascular angina than in normal volunteers (16 +/- 8.6 versus 22.2 +/- 3.7, p = 0.026). We conclude that airway hyperresponsiveness is frequently demonstrable in patients with microvascular angina; these findings are consistent with our hypothesis that this syndrome may represent a more generalized abnormality of vascular and nonvascular smooth muscle function.

Adult↗

PubMed1996

[Diastolic left ventricular dysfunction with microvascular angina (Syndrome X)].

Findings on left ventricular function in microvascular angina (syndrome X) are somewhat controversial. Recently, an increased prevalence of insulin resistance and hyperlipoproteinemia has been demonstrated as well as arterial hypertension potentially impairing the left ventricular diastolic function. In an attempt to analyze the diastolic function at rest, we investigated by Doppler echocardiography the transmitral blood flow in 16 patients (51 +/- 8 years). The diastolic data were compared with those of 12 healthy people (50 +/- 6 years) who were matched for age. The patients with microvascular angina revealed a slightly higher systolic blood pressure (134 +/- 18 mm Hg vs 125 +/- 9 mm Hg, n.s.), but imposed by higher left ventricular mass index (92 +/- 18 g/m2 vs 65 +/- 13 g/m2, p < 0.001). There was a trend to an elevated A-wave-peak during transmitral blood flow (61 +/- 14 cm/s vs 50 +/- 9 cm/s). The findings suggest impairment of the left ventricular relaxation before manifestation of left ventricular hypertrophy and hypertension takes place.

Adult↗

PubMed2005

Microvascular angina, adverse outcome: a case report.

We encountered a patient with microvascular angina (MVA) who was died suddenly, and observed ST-segment elevation during attack without epicardial coronary arterial vasoconstriction, suggesting the occurrence of microvascular spasm. Doppler guide wire (DGW) and N-13 ammonia positron emission tomography (PET) demonstrate severe impairment of the coronary microcirculation extending throughout the whole of the left ventricle. Conventional medical treatment was not effective in this case. We speculate that the prognosis of microvascular angina with severe coronary microcirculatory disturbance and accompanied by microvascular spasm might not always be good. Therefore, methods for treating such cases need to be established.

Adult↗

PubMed1995

[The significance of insulin resistance and hyperlipidemia in microvascular angina (syndrome X)].

Patients with chest pain and normal epicardial coronary arteries are characterized by an impairment of myocardial perfusion reserve. Functional and morphological abnormalities of the intramyocardial arterioles are suggested to be responsible for this, possibly as a consequence of hypertension and/or left ventricular hypertrophy. In an attempt to isolate predisposing factors of microvascular angina we investigated 34 patients (15 f, 19 m) with a mean age of 53 +/- 7 years. They were diagnosed as microvascular angina without hypertension or left ventricular hypertrophy. Parameters such as plasma insulin, glucose, cholesterol, LDL-cholesterol, triglycerides, (VLDL-cholesterol) and fibrinogen were determined for a metabolic profile. Furthermore, insulin and glucose were measured after an oral glucose load of 100 g glucose (OGTT) over 3 h. All parameters were compared to a control group of 15 healthy people matched for age and body mass index. In the study population systolic blood pressure was within normal limits at 137 +/- 17 mm Hg and thus higher than control at 124 +/- 11 mm Hg (p < 0.02). Furthermore, diastolic blood pressure was 85 +/- 7 mm Hg compared to 78 +/- 9 mm Hg in controls (p < 0.02). Insulin was significantly elevated in patients with microvascular angina 90 min (median: 101 vs 54 microU/ml; p < 0.01) and 120 min (median: 88 vs 51 microU/ml; p < 0.05) after ingestion of 100 g glucose. The fasting glucose was elevated at 98 +/- 12 compared to 87 +/- 7 mg/dl in controls (p < 0.01). Glucose concentration was also elevated after 30 min at 176 +/- 28 compared to 148 +/- 32 mg/dl (p < 0.02), after 45 minutes (198 +/- 35 compared to 152 +/- 53 mg/dl) (p < 0.01) and 60 minutes (193 +/- 44 compared to 145 +/- 54 mg/dl) (p < 0.01). In microvascular angina parameters such as total cholesterol: (244 +/- 46 vs 199 +/- 29 mg/dl (p < 0.01)), LDL-cholesterol (157 +/- 41 vs 122 +/- 18 mg/dl (p < 0.01)) and fibrinogen: (377 +/- 150 vs to 285 +/- 69 mg/dl (p < 0.03)) were elevated. These findings suggest a pathogenetic role of insulin resistance, hyperlipoproteinemia and elevated levels of fibrinogen for impaired myocardial coronary reserve. This metabolic constellation as well as exhaustion of coronary reserve is often found in hypertensive patients and may identify microvascular angina as an early stage of hypertensive heart disease before manifest hypertension has developed.

Adult↗

PubMedDate not supplied

Nitric oxide synthase gene G298 allele. Is it a marker for microvascular angina in hypertensive patients?

BACKGROUND: Nitric oxide (NO) has an important effect on blood pressure, arterial wall, and the basal release of endothelial NO in hypertension (HPN) may be reduced. Until now, there is no solid data revealing the potential role of the polymorphism of the nitric oxide synthase gene (NOS) in patients with HPN and microvascular angina. AIM: The aim of the present study is to investigate the gene of endothelial nitric oxide synthase (eNOS), as the polymorphism of this gene may be a putative candidate for HPN and initiate the process of atherosclerosis. METHODS: Sixty participants were recruited for this study; 50 were hypertensive patients complaining of chest pain [30 of them have electrocardiogram (EKG) changes of ischemia], 20 had isolated HPN, and 10 healthy volunteers served as control. All patients underwent stress myocardial perfusion imaging (MPI) and coronary angiography. Genotyping of eNOS for all patients and controls was performed. The linkages between HPN, microvascular angina and eNOS gene polymorphism were investigated. RESULTS: MPI and coronary angiography revealed that 15 patients had chest pain with true ischemia and reversible myocardial perfusion defects (multiple and mild) but normal epicardial coronary arteries (microvascular angina), while 15 patients had significant coronary artery disease (CAD), and 20 hypertensive patients showed normal perfusion scan and coronary angiography. The prevalence of the NOS G(298) allele was higher in the hypertensive group with microvascular angina (documented by MPI) than it was among the control participants (P<.005). The eNOS allele was significantly higher in the hypertensive group than in the control participants, but there was no significant difference in homozygote mutants among hypertensive participants, x-syndrome and patients with CAD. CONCLUSION: eNOS gene polymorphism is proved to be an important etiology in microvascular angina (x-syndrome) among hypertensive patients. In addition, the eNOS mutant gene showed a significant increase in isolated HPN and in patients with CAD.

Alleles↗

PubMed1994

[Long-term antihypertensive therapy with isradipine. Improvement of coronary flow reserve in patients with arterial hypertension and microvascular angina].

Antihypertensive Long-term Therapy with Isradipine/Improvement of coronary flow reserve in patients with arterial and microvascular angina In patients with arterial hypertension coronary flow reserve is often impaired due to left ventricular (LV) hypertrophy and alterations of the coronary microcirculation. Experimental and clinical studies have shown that calcium channel blockers can induce regression of myocardial hypertrophy. Objective of the present study was to see whether chronic antihypertensive treatment with calcium channel blockers can improve the diminished coronary reserve in patients with arterial hypertension and microvascular angina pectoris. Fifteen hypertensive patients with microvascular angina (61 +/- 7 years, normal coronary angiogram, mild LV-hypertrophy) were treated with isradipine (CAS 75695-93-1) (5.3 +/- 0.9 mg/d) for 12 +/- 2 months. Before and after therapy (after a washout period of 1 week) coronary flow was quantitatively measured by the gas chromatographic Argon method. Coronary reserve was calculated as the quotient of coronary resistance under baseline conditions and after dipyridamole (0.5 mg/kg i.v.). Under isradipine therapy systolic blood pressure was lowered from 165 +/- 20 to 140 +/- 13 mmHg (p < 0.01) and diastolic blood pressure from 98 +/- 8 to 88 +/- 6 mmHg (p < 0.01). The LV muscle mass index decreased by 10% from 154 +/- 33 to 139 +/- 28 g/m2 (p < 0.05). Baseline coronary blood flow (81 +/- 13 versus 83 +/- 16 ml/min x 100 g, n.s.) was identical before and after therapy. There were also no differences in coronary perfusion pressure, heart rate, myocardial oxygen consumption and arterio-coronary venous oxygen difference before and after therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1993

Insulin resistance, glucose intolerance, and hyperinsulinemia in patients with microvascular angina.

Plasma glucose and insulin responses to oral glucose and insulin-mediated glucose disposal were determined in 20 patients with microvascular angina and 20 normal volunteers who were similar in terms of age, gender distribution, and degree of obesity. Plasma glucose and insulin responses to a 75-g oral glucose challenge were significantly higher in those with microvascular angina (P < .001), as were steady-state plasma glucose concentrations after a 180-minute infusion of somatostatin, glucose, and insulin (12.2 +/- 1.0 v 7.6 +/- 0.6 mmol/L, P < .001). Since steady-state plasma insulin concentrations were similar in the two groups (627 +/- 32 v 631 +/- 29 pmol/L), these data indicate that patients with microvascular angina are insulin-resistant, glucose-intolerant, and hyperinsulinemic compared with a matched group of normal volunteers.

Blood Glucose↗

PubMed1995

Insulin-resistant glucose metabolism in patients with microvascular angina--syndrome X.

Studies in patients with microvascular angina (MA) or the cardiologic syndrome X have shown a hyperinsulinemic response to an oral glucose challenge, suggesting insulin resistance and a role for increased serum insulin in coronary microvascular dysfunction. The aim of the present study was to examine whether patients with MA are insulin-resistant. Nine patients with MA and seven control subjects were studied. All were sedentary and glucose-tolerant. Coronary arteriography was normal in all participants, and exercise-induced coronary ischemia was demonstrated in all MA patients. A euglycemic, hyperinsulinemic clamp was performed in combination with indirect calorimetry. Biopsy of vastus lateralis muscle was taken in the basal state and after 4 hours of euglycemia and hyperinsulinemia (2 mU.kg-1.min-1). The fasting level of "true" serum insulin was significantly higher (43 +/- 6 v 22 +/- 3 pmol/L, P < .02) and the rate of insulin-stimulated glucose disposal to peripheral tissues was lower in patients with MA (13.4 +/- 1.0 v 18.2 +/- 1.4 mg.kg fat-free mass [FFM]-1.min-1, P < .02) due to a decrease in nonoxidative glucose metabolism (8.4 +/- 0.9 v 12.5 +/- 1.3 mg.kg FFM-1.min-1, P < .02). No difference was found in glucose or lipid oxidation rates between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2000

[Results of myocardial scintigraphy with 99mTc-tetrofosmin and dipyridamole administration in patients diagnosed of microvascular angina].

The objective of the study was to evaluate the results of the myocardial scintigraphy with 99mTc-tetrofosmin (Tc-Tf) and pharmacological stimulation with dipyridamole in patients diagnosed of microvascular angina. The study population is made up of 50 patients discharged with the diagnosis of microvascular angina who had undergone Tc-Tf-dipyridamole. Clinical and electrical positivity appeared in 40% and 12% of the patients, respectively. Myocardial perfusion defects were found in 35 patients (70%), and were reversible in 21 (60%), fixed in 11 (21%), and combined in 3 (9%). Abnormalities were inferior, anteroseptal and lateral in 21, 18, and 2 patients, respectively. Patients with a positive exercise treadmill test, compared with those with a negative one, had more frequent perfusion abnormalities (91% vs 50%, p = 0.0327) and myocardial ischemia (64% vs 20%, p = 0.392). Women, in comparison with men, had angina (56% vs 22%, p = 0.013), and anteroseptal perfusion abnormalities (26% vs 4%, p = 0.028) more frequently. On the contrary, men had inferior perfusion abnormalities more frequently (57% vs 30%, p = 0.057). Thus, Tc-Tf-dipyridamole shows perfusion abnormalities in 70% of patients with microvascular angina (91% in patients with a positive exercise treadmill test). Scintigraphic pattern may be partially conditioned by gender in these patients.

Coronary Circulation↗

PubMed1995

[Microvascular angina pectoris and insulin resistance].

The authors examined 29 patients with the syndrome of microvascular angina pectoris. In 12 patients (41.4%) they recorded hyperinsulinaemia as a manifestation of insulin resistance. The body weight, HDL cholesterol level, LDL cholesterol and triglycerides did not differ significantly in the two groups and were at the upper borderline of the range of reference values. The authors analyze mechanisms common to the pathophysiology of the syndrome of microvascular angina pectoris and the syndrome of insulin resistance.

Adult↗

PubMed1991

Comparison of exercise testing with studies of coronary flow reserve in patients with microvascular angina.

Abnormal small coronary artery function may cause limited coronary flow responses to stress, resulting in anginal symptoms and ischemia in some patients with chest pain despite angiographically normal coronary arteries. To assess the exercise hemodynamic correlates of coronary flow abnormalities measured in the cardiac catheterization laboratory, 105 patients with microvascular angina (defined as an increase in coronary vascular resistance during pacing stress after ergonovine administration in the absence of significant epicardial constriction and associated with provocation of the patient's typical chest pain) and 27 patients without any coronary flow abnormality (normal) were analyzed. Of the 105 patients with microvascular angina, 75 had normal electrocardiographic responses to treadmill exercise testing, 22 had ischemic responses, and eight had bundle branch block during exercise. All 27 normal patients had normal electrocardiographic responses to exercise. Patients with ischemic electrocardiographic responses (0 +/- 7%, p less than 0.01), and those with bundle branch block (-2 +/- 6%, p less than 0.01) had abnormal left ventricular ejection fraction responses to exercise compared with the normal group, who demonstrated an 8 +/- 6% increase in left ventricular ejection fraction by radionuclide angiography during exercise, and microvascular angina patients with a normal electrocardiographic response to exercise, who demonstrated a 5 +/- 7% increase in ejection fraction. Although the microvascular response to ergonovine was no different among the three microvascular angina exercise groups, the administration of dipyridamole caused less coronary vasodilation in those patients with apparently ischemic or bundle branch block responses to exercise compared with those with normal electrocardiograms during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗

PubMed2002

Adenosine provokes diastolic dysfunction in microvascular angina.

Adenosine stress echocardiography was performed in nine patients (58 (+/-3) years, eight women) with documented microvascular angina. Global ventricular function was assessed by Tc(99m) blood pool imaging and Doppler, whereas longitudinal ventricular function was assessed by simultaneous tissue Doppler echocardiography of the lateral mitral annulus. Adenosine was infused incrementally to onset of chest pain in all patients. There was no significant change in global or longitudinal systolic function. Adenosine induced global diastolic dysfunction, demonstrated by blood pool imaging and by Doppler of the transmitral flow. All patients had long axis diastolic dysfunction at peak adenosine, revealed by a ratio of early to late diastolic velocity of lateral mitral annulus <1, which was absent at rest. Adenosine, as a stress agent, provokes regional and global diastolic dysfunction in microvascular angina, which may be a consequence of subendocardial ischaemia. Long axis diastolic dysfunction can be easily revealed by tissue Doppler of the lateral annular motion.

Adenosine↗