SEARCH · PubMed Health

Results for “Microvascular Angina”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

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↗

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↗

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↗

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↗

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↗

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↗

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↗

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↗

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↗