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Results for “Microvascular Angina”

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PubMed1990

Beneficial and detrimental effects of lidoflazine in microvascular angina.

Lidoflazine, a piperazine derivative calcium antagonist, was investigated as therapy in 22 patients with microvascular angina (chest pain, angiographically normal coronary arteries and left ventricle, microvascular constrictor response to pacing after ergonovine administration and limited coronary flow response to dipyridamole). Eighteen of 22 patients reported symptom benefit while taking lidoflazine 360 mg daily. Compared to baseline exercise treadmill testing, lidoflazine resulted in significant improvement in exercise duration (812 +/- 337 vs 628 +/- 357 seconds, p less than 0.01) and time to onset of chest pain (530 +/- 343 vs 348 +/- 246 seconds, p less than 0.01). The 5 patients with ischemic ST-segment changes during baseline testing demonstrated an almost 4-minute delay in ST-segment depression (3 patients) or no ST-segment depression (2 patients) while taking lidoflazine. Repeat invasive study of coronary flow in 11 patients taking lidoflazine demonstrated significantly greater coronary vasodilation at rest, during pacing, during pacing after ergonovine and after dipyridamole administration (all p less than 0.03), compared to the initial drug-free study. During the randomized, placebo-controlled phase of the study with 7-week treatment periods, 9 of 11 patients who completed this phase of the study preferred lidoflazine and all demonstrated improved exercise capacity with lidoflazine compared to placebo. However, 3 patients developed malignant ventricular arrhythmias, and 1 died while taking lidoflazine, resulting in termination of the study. Limited coronary vasodilator response in microvascular angina has a reversible vasoconstrictor component and may be due to elevated systolic calcium levels. Despite the hemodynamic, symptom and exercise benefit, lidoflazine may be unsafe for clinical use because of its propensity to cause potentially fatal ventricular arrhythmias.

Adult↗

PubMed2005

Relation between Duke treadmill score and coronary flow reserve using transesophageal Doppler echocardiography in patients with microvascular angina.

OBJECTIVES: The link between coronary flow reserve (CFR) and Duke treadmill score (DTS) in patients with microvascular angina remains elusive. METHODS: We studied 108 subjects (M/F=48:60, mean age 54+/-9 years) with chest pain and normal coronary angiogram. ETT was performed by Bruce's protocol and the equation for calculating DTS was DTS=exercise duration-(5x ST deviation)-(4x exercise angina), with 0=none, 1=nonlimiting, 2=exercise limiting. The coronary flow velocity at diastole (PDV) using transesophageal Doppler echocardiography (TEE) was obtained from the proximal left anterior descending coronary artery and CFR was calculated as the ratio of hyperemic PDV after the intravenous infusion of dipyridamole (0.56 mg/kg) to baseline PDV. RESULTS: CFR was 3.04+/-0.45 in group with negative ETT and 2.19+/-0.62 in group with positive ETT (P<0.001) and was 1.51+/-0.31 in high risk group with a score of < or = -11, 2.39+/-0.63 in moderate risk group with scores between -11 and + 5, and 3.04+/-0.43 in low risk group with a score of > or = +5 on DTS (P<0.001 versus low risk group, respectively). DTS has significant correlation with CFR (r=0.704, P<0.001). CONCLUSIONS: DTS is a composite index that reflects CFR and helps clinicians determine the severity of ischemia in patients with microvascular angina.

Adult↗

PubMed1997

Enhanced red cell sodium-hydrogen exchange in microvascular angina.

OBJECTIVES: Enhanced calcium content in arterial smooth muscle cells and altered reactivity of coronary vessels to alkalinization have been reported in angina pectoris due to impaired motility of coronary arteries. An altered function of sodium-hydrogen exchange, a ubiquitous membrane transport system that links proton efflux to calcium drifts, may mediate these phenomena. DESIGN AND SUBJECTS: Twenty patients with microvascular angina (stable effort angina, reversible perfusion defects during effort thallium 201 heart scintigraphy, and angiographically normal coronary arteries) were compared to 20 patients with stable effort angina due to coronary atherosclerosis and 20 healthy subjects. The sodium-hydrogen exchange was defined as the initial fraction of the amiloride-sensitive proton efflux from red cells with inhibited anion exchanger (pHi 6.00-6.05) into an Na(+)-containing medium (pHo 8.00-8.05). 12-0-tetradecanoylphorbol-13-acetate (TPA, 600 nmol.l-1) and staurosporine (100 nmol.l-1) were used as phosphorylation modulators in vitro. RESULTS: The mean red blood cell Na+/H+ exchange was increased in patients with microvascular angina (451 +/- 37 vs 142 +/- 17 and 124 +/- 21 umol H+.1 cells-1.min-1, P < 0.01). TPA and staurosporine abolished differences between the groups. CONCLUSIONS: Microvascular angina is associated with enhanced Na+/H+ exchange in erythrocytes, probably due to more extensive phosphorylation of the membrane antiporter sites.

Cell Membrane↗

PubMed1994

Small vessel pathology and coronary hemodynamics in patients with microvascular angina.

We studied the ultrastructure of cardiac myocytes and small blood vessels obtained by endomyocardial biopsy from 21 patients with microvascular angina. Ischemic ST segment depression during atrial pacing was recognised in all the patients who had normal coronary arteriograms and biopsy tissues were examined by light and electron microscopy. In patients with microvascular angina, insufficient increases in coronary sinus blood flow and in myocardial oxygen consumption measured with a Webster's catheter were apparent during atrial pacing. Biopsy samples under the light microscope showed evidence of myocardial hypertrophy and sclerosis of small arteries and arterioles with perivascular fibrosis in 18 of 19 (95%) patients. Electron microscopy revealed that many endothelial nuclei in capillaries were swollen and that lumina of small arteries and arterioles were irregularly narrowed with proliferated and deformed medial smooth muscle cells. These findings suggest that disturbances in the coronary microcirculation in these patients is responsible for the ischemic changes in electrocardiograms.

Aged↗

PubMed1996

[Impairment of myocardial perfusion reserve in microvascular angina (syndrome X): assessment by 99mTc-MIBI-SPECT].

AIM: In 22 patients with typical chest pain and normal coronary arteries (microvascular angina, syndrome X) 99mTc-MIBI-SPECT was examined in regard to assess impairment of myocardial perfusion reserve. METHOD: The study was performed with 99mTc-MIBI-SPECT at rest and under vasodilation with dipyridamole. The findings were compared with a normal database. A normal perfusion reserve was said to be an increase > 20% of the 99mTc-MIBI-activity. RESULTS: In 2/22 (9%) of the patients the perfusion reserve lay > 20% i.e. 37%. In 91% of the patients a diminution or even decrease of the perfusion was to be seen. From these 9/22 (41%) of the patients showed a diminution of the 99mTc-MIBI-uptake by 6%. 1/22 patients had a decrease of the perfusion under vasodilation with dipyridamole i.e. a lower activity of 99mTc-MIBI by 13% CONCLUSION: Vasodilation 99mTc-MIBI-SPECT offers good imaging quality and enables semi-quantitative assessment of myocardial perfusion reserve in patients with microvascular angina.

Blood Pressure↗

PubMed2000

Microvascular angina in patients with syndrome X.

Syndrome X (SX) is usually diagnosed in the presence of angina and normal coronary arteriograms. It is an heterogeneous syndrome which encompasses different pathogenic mechanisms. Whether myocardial ischaemia is responsible for the condition remains controversial. The term "microvascular angina" has been used to define the syndrome of chest pain and normal coronary arteries with heightened sensitivity of the coronary microcirculation to vasoconstrictor stimuli. It has been suggested that the abnormal vasodilator response of the coronary circulation in patients with SX is due to impaired endothelial function. Plasma levels of endothelin in patients with chest pain and normal coronary arteries were found to be significantly raised compared to normal controls. Endothelial dysfunction in SX is likely to be multifactorial and many cardiac risk factors, such as hypertension, hypercholesterolemia, oestrogen deficiency and smoking, can contribute to its development. As the majority of SX patients are women and most are post-menopausal, oestrogen deficiency has been proposed as a pathogenic factor. A large proportion of patients satisfying the stated criteria for SX have one or more coronary risk factors. Additional factors, such as abnormal pain perception, may contribute to the evolution of chest pain in patients with normal coronaries and endothelial dysfunction. Combined alteration of pain perception and microvascular dysfunction are likely to explain a proportion of all cases of SX. The treatment of this syndrome represents a major challenge for the cardiologist. Beta-blockers and calcium channel blockers are effective in controlling chest pain in SX patients. A very important therapeutic intervention in microvascular angina is the control of risk factors that can lead to endothelial dysfunction. Different approaches, including spinal cord stimulation and psychological treatment, have been proposed especially for those patients in whom a cardiac origin of pain is unlikely.

Antidepressive Agents, Tricyclic↗

PubMed2002

[Microvascular angina and syndrome X].

Cardiac syndrome X defines patients with typical chest pain, transient ischaemic ST segment changes during effort and normal coronary angiograms. An ischaemic origin has been postulated for syndrome X since its description over 30 years ago. This has been based on the fact that patients with cardiac syndrome X have abnormal perfusion scans, a drop in both pH and oxygen saturation of the coronary sinus blood during chest pain and transmyocardial lactate production during stress testing. Moreover, nuclear magnetic resonance spectroscopy studies, demonstrated transient myocardial ischaemia in 20% of women with syndrome X. Microvascular endothelial dysfunction appears to be responsible for at least some of the abnormalities detected in the coronary circulation of patients with syndrome X ("microvascular angina"). ET-1, a potent vasoconstrictor, is synthesised by endothelial cells and may be responsible for coronary flow abnormalities in microvascular angina. Plasma levels of ET-1 are significantly raised in patients with syndrome X, compared to normal controls and a significant relationship has been found between baseline ET levels and abnormal coronary vascular responses in patients with syndrome X. Several investigators, however, have questioned the existence of myocardial ischaemia in patients with cardiac syndrome X. Their arguments are mainly based on the fact that prognosis is good in these patients and that studies with stress echocardiography have consistently failed to show regional wall motion abnormalities, even in patients with typical ischaemic ECG changes. Controversy exists as to the causes of syndrome X and this article reviews the evidence in relation to myocardial ischaemia as a pathogenic mechanism in this syndrome.

Endothelins↗

PubMed2000

[Thallium scintigraphy of the myocardium in evaluation of patients with insulin resistance syndrome and microvascular angina pectoris].

Insulin resistance syndrom (IR) is often associated with the syndrome of microvascular angina pectoris (MVAP) or with coronary artery disease (CAD). The authors quantified distribution and washout of 201Tl in heart (C), lungs (L) and liver (H) to evaluate the results 201Tl stress (s) and redistribution SPECT in 50 patients. They compared 2 groups of patients with laboratory verified IR (MVAP and CAD) and control group (CG) of patients with normal coronarography without any symptoms of IR. In Patients with IR and MVAP were found significantly more frequent local perfusion abnormalities then in CG. The index sL/C calculated by ROI analysis is significantly lower in controls, then in CAD. The index sC/H is lower in patients with IR (MVAP significantly) then in CG. The washout of 201Tl in CAD myocardium decreased and in MVAP liver increased. 201thalium scintigraphy is useful for separation of patients with MVAP and local perfusion abnormalities. This findings had probably prognostic value in patients with IR.

Coronary Circulation↗

PubMed1991

Exercise testing in patients with microvascular angina.

The widespread use of exercise testing for the detection of myocardial ischemia in patients suspected of having coronary artery disease led to the detection of ischemic changes in many subjects who subsequently were found to have angiographically normal epicardial vessels--the false positive response. Such a result is usually interpreted as indicating that the subject's chest pain is of noncardiac origin. For the past several years, we have studied the mechanism of pain resembling angina that occurs in patients with normal epicardial coronary arteries demonstrated by angiography; we believe these studies have shed some light on this problem. Patients with angiographically normal coronary arteries who present because of a history of angina-like pain and/or ischemic changes detected during exercise electrocardiogram testing were evaluated by measuring great cardiac vein flow (under baseline conditions and after cardiac pacing, with and without intravenous administration of ergonovine) and by radionuclide angiography before and during exercise. We found that a substantial number of these subjects showed inadequate coronary vasodilator reserve and had exercise-induced left ventricular dysfunction suggestive of myocardial ischemia. We concluded from our results that there is a distinct clinical syndrome of myocardial ischemia caused by abnormal resistance responses of the prearteriolar coronary microvasculature. We now refer to this syndrome as microvascular angina. In a series of 115 patients with documented microvascular angina, we also found that only 10% had ischemic ST changes with exercise testing (2% of the men and 17% of the women developed ischemic ST segment changes).(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗

PubMed2002

Microvascular angina accompanied by epicardial coronary artery spasm.

A case of microvascular angina accompanied by coronary artery spasm is described. A 54-year-old woman had anginal pain at rest and during exercise. Both exercise testing and rapid atrial pacing caused significant ST depression in the inferior and all precordial leads. Exercise thallium myocardial scintigraphy was negative despite similar ST depressions. Coronary angiography revealed insignificant stenoses of the left anterior descending coronary artery after the injection of nitrate. Intracoronary acetylcholine provoked diffuse spasm of the artery with concurrent myocardial lactate production. Coronary flow reserve assessed with papaverine was 2.75. The combined use of amlodipine and high-dose nicorandil was effective for the treatment of angina.

Angina Pectoris↗

PubMed1987

Impaired forearm vasodilator reserve in patients with microvascular angina. Evidence of a generalized disorder of vascular function?

In previous work, we described a group of patients with angina-like chest pain and normal coronary arteries. These patients had impaired coronary vasodilator responses to the stress of rapid atrial pacing and to the administration of dipyridamole, a potent vasodilator of coronary arterioles. This abnormality appears to be localized to the prearteriolar microvascular bed. To determine whether these patients have a more generalized abnormality of vasodilator reserve, we used mercury-in-Silastic strain-gauge plethysmography to compare their hyperemic responses to forearm ischemia with those of normal controls. After 10 minutes of ischemia, peak forearm flow was 39.9 +/- 5.0 ml per minute per deciliter in the controls [corrected] and 31.7 +/- 10.5 in the patients [corrected] (21 percent reduction; 95 percent confidence interval, 4 percent to 37 percent). Flow responses were also significantly reduced after three and five minutes of ischemia. Correspondingly, the vascular resistance after ischemia was also consistently higher in the patients with microvascular angina. The degree of vasodilator impairment in the peripheral circulation correlated well with the degree of vasodilator impairment in the coronary circulation (r = 0.74; P less than 0.004). Thus, patients with microvascular angina appear to have an impairment of vasodilator reserve that affects not only their coronary circulation but also their peripheral arterial bed.

Adult↗

PubMed1995

Ultrastructural changes of blood capillaries in patients with microvascular angina, hypertrophic cardiomyopathy, and dilated cardiomyopathy.

Blood capillary abnormalities accompanied by intramural small arterial lesions were reported in patients with microvascular angina (MVA), hypertrophic cardiomyopathy (HCM), and dilated cardiomyopathy (DCM). We compared the ultrastructural changes of blood capillaries in myocardial biopsy samples from MVA, HCM, and DCM patients using electron microscopy and ultrastructural morphometry. Ten cross-sectioned views were selected from each patient at random, and the degree of cytoplasmic swelling of the endothelial cells was measured (transverse area of endothelial cell cytoplasm (E)/transverse area of the blood capillary (C)). The thickness of the basal lamina was also assessed (transverse area of basal lamina (BL)/C). The average value of the E/C ratio was in the order of control group < HCM < MVA < DCM, with significant differences among the groups (p < 0.001). The average value of the BL/C ratio was in the order of control group < MVA < HCM < DCM, with significant differences (p < 0.001) among the groups except between the HCM and DCM groups. In conclusion, swelling of the endothelial cells as well as luminal stenosis of small arteries and arterioles may be related to disturbed microcirculation in these patients.

Adult↗

PubMed2001

Microvascular angina in a patient with aortic stenosis.

A 39-year-old woman had exercise-induced ST segment depression associated with chest pain. Cardiac evaluation revealed moderate aortic stenosis (AS), related to the bicuspid valves, with an aortic mean pressure gradient of 22 mmHg, a calculated aortic valve area of 1.3 cm2 and normal left ventricular (LV) peak systolic and end-diastolic pressures, but no LV hypertrophy, resulting in normal LV wall stress. Although the coronary arteries were angiographically normal, rapid atrial pacing and an intracoronary papaverine injection revealed a significantly decreased coronary flow reserve (CFR), which may have played an important role in the pathogenesis of angina pectoris in this patient. Though the CFR is usually decreased in patients with AS, as well as in microvascular angina, in this particular case, it appeared to have decreased as a consequence of microvascular dysfunction rather than of AS-related mechanisms.

Adult↗

PubMed1995

Microvascular angina in patients with normal coronary arteries and with other ischaemic syndromes.

In this paper we review the evidence that angina and 'ischaemic' ST depression can be caused by inappropriate constriction of small coronary artery vessels in patients with microvascular angina (i.e. anginal chest pain with angiographically normal coronary arteries). Although the mechanisms responsible for microvascular dysfunction remain unknown, it is conceivable that the constrictor stimuli may involve vessels which are proximal to those involved in metabolically induced dilation, so that the effect cannot be opposed, at the same site, by the dilator effect caused by ischaemic metabolites. Furthermore, in this review we also present evidence that myocardial ischaemia may result mainly from inappropriate constriction of small coronary vessels, rather than by obstruction of major epicardial coronary arteries. In addition, there are those prone to the condition, such as specific groups of patients with atherosclerotic ischaemic syndromes, including patients with single isolated coronary artery occlusion and no evidence of previous myocardial infarction, patients with single-vessel coronary stenosis who underwent successful balloon angioplasty, and patients with single-vessel disease with detectable abnormal vasomotor responses in non-stenotic coronary arteries.

Adenosine↗

PubMed1989

Microvascular angina and panic disorder.

Recent cardiac studies have suggested that patients with chest pain and angiographically normal coronaries have "microvascular angina" (MVA). In contrast, prior psychiatric studies have shown that some of these patients have panic disorder (PD). We compared the clinical and psychologic characteristics of fifteen patients with MVA and fifteen patients with panic disorder (PD), and examined response to lactate infusion in a subgroup of MVA patients. Although 40 percent of MVA patients met criteria for PD and had chest pain following lactate infusion, there were psychologic and symptomatic differences between the MVA and PD groups. These results reflect either co-morbidity of MVA and PD in some patients or two types of MVA, one of primary cardiac origin and one a centrally mediated epiphenomenon of the increased autonomic arousal seen in PD.

Agoraphobia↗

PubMed1993

[Global and regional function in microvascular angina].

Because of the existing relation between myocardial blood flow and systolic function, various noninvasive techniques, capable of assessing regional and global left ventricular function, especially two-dimensional echocardiography, have been used in patients with chest pain, ECG evidence of myocardial ischemia and/or reduced coronary flow reserve and angiographically detected normal coronary vessels. The results, however, have been contradictory, while only few of them have reported stress-induced regional or global left ventricular dysfunction combined with ST-segment depression and/or angina. The reason for such discrepancy could be due to a diffuse but patchy distribution of myocardial ischemia, or to a non-ischemic origin of the clinical and instrumental features of this syndrome, relying on the effect of algogenic mediators, as suggested from recent metabolic studies. Even if the most recent theories agree on the functional involvement of the small coronary vessels, many points on microvascular angina remain confused. An agreement on the nosological classification of this syndrome would be welcome, given the high technological cost required for the study of coronary microcirculation.

Humans↗

PubMed1999

Regional Diastolic Function in Microvascular Angina Studied by Pulsed-Wave Doppler Tissue Imaging.

OBJECTIVES: Diastolic dysfunction is an early finding during myocardial ischemia. However, regional diastolic function has not been studied in patients with microvascular angina (MA). The purpose of this study was to assess the regional diastolic function in patients with MA through use of the new echocardiographic technique, pulsed-wave Doppler tissue imaging (DTI). METHODS: Regional diastolic function was studied by DTI in 81 myocardial segments of seven patients with MA and in 54 segments of six healthy control subjects. RESULTS: Myocardial segments in patients with MA had, in comparison with controls, an increased regional isovolumetric relaxation time (126 +/- 34 vs 99 +/- 34 msec, P < 0.0001), a higher e/a ratio (1.1 +/- 0.7 vs 0.8 +/- 0.3, P = 0.0048), and a lower peak velocity of the late diastolic wave a (6.9 +/- 2.9 vs 8.4 +/- 1.7 cm/msec, P = 0.0009). Moreover, peak velocity of systolic wave s was higher in patients with MA (5.8 +/- 1.4 vs 5.3 +/- 1.2 cm/msec, P = 0.0424). CONCLUSIONS: Patients with MA have an impaired regional diastolic function (an increased regional isovolumetric relaxation time and a lower a wave) and a higher velocity of the regional systolic wave s. These findings may have physiopathological implications.

Journal Article↗

PubMed2001

Cardiac amyloidosis presenting as microvascular angina--a case report.

Cardiac amyloidosis usually presents with heart failure, but rarely leads to coronary insufficiency. The authors report a case of a 69-year-old Japanese woman with cardiac amyloidosis presenting as microvascular angina. She had exertional angina with positive exercise test and normal coronary angiograms. However, heart failure developed, and she died 3 years after symptom onset. On autopsy, coronary arteries were patent. In contrast to that of the epicardial coronary arteries, histologic examination of the heart revealed severe obstructive alterations of the intramural coronary arteries with amyloid. Furthermore, amyloid was present mainly in the endocardium and the intramural coronary arteries, but there was little present in the myocardium. This case was a rare AL amyloidosis. There have been only 4 reported cases of cardiac amyloidosis that presented with exertional angina, a positive exercise test, and normal coronary angiograms and histologic examination.

Aged↗