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PubMed1994

[Flecainide exercise induced left bundle branch with chest pain].

Ischaemia has been the suggested mechanism of simultaneous left bundle branch block and chest pain on effort with normal coronary angiography. This hypothesis is very controversial and was not the mechanism in the two new cases of this syndrome. The two patients in whom effort pain and left bundle branch block were observed had been treated for paroxysmal supraventricular tachycardia with flecaine. Withdrawal of the anti-arrhtymic resulted in the disappearance of this syndrome. In these cases, the ischaemic mechanism could be excluded without ambiguity. The flecaine was the only cause of rate-related LBBB by slowing conduction in the left bundle branch with no effects on coronary reserve. It would seem that LBBB alone was the cause of chest pain. The absence of coronary artery disease was confirmed in the first patient and the diagnosis was highly improbable in the second.

Aged↗
PubMed1996

Abnormal coronary flow reserve in patients with angina pectoris and hypertensive left ventricular hypertrophy.

OBJECTIVE: To assess coronary flow reserve using a computer-assisted method with intracoronary papaverine in patients with angina pectoris. PATIENTS AND METHODS: Coronary arterial diameter, cross-sectional area and blood flow velocity were measured during coronary arteriography before and after intracoronary papaverine in 26 control subjects, 45 patients with significant coronary artery disease (> 50% luminal narrowing), 16 patients with syndrome X and 14 patients with hypertension and left ventricular hypertrophy (LVH). RESULTS: After intracoronary administration of papaverine, proximal diameter, cross-sectional area, blood velocity, flow volume and reserve capacity of both left anterior descending and right coronary arteries were lower in patients with significant coronary stenosis than in the controls. Despite similar changes in diameter and cross-sectional area, the blood velocity, flow volume and reserve capacity of the two vessels were also lower in patients with syndrome X than in the controls. In 14 patients with hypertension and LVH, although the blood velocity and flow volume were augmented for the two arteries and did not differ from those in the controls, the flow reserve was reduced because of higher baseline blood velocity and flow volume. CONCLUSIONS: Coronary flow reserve is reduced in patients with coronary artery disease, syndrome X or hypertensive LVH, which may be related to abnormal changes at different levels of the coronary vasculature or resting flow states.

Angina Pectoris↗
PubMed1994

X-syndrome: is there impairment of myocardial perfusion during stress?

Stress T1-201 myocardial scintigraphy was carried out in 16 patients with x-syndrome. Eleven patients having IHD with single-vessel disease served as the control. With bicycle exercise test all 16 patients with x-syndrome had some type of myocardial perfusion abnormality. These perfusion defects were situated in the vascular beds of different coronary arteries. Myocardial perfusion defects in patients with x-syndrome were similar to those patients with moderate, but haemodynamically significant, single-vessel disease. At the same time, these perfusion defects were significantly less pronounced than those in patients with a subtotal occlusion of one coronary artery. Thus, patients with x-syndrome have not only the clinical features of IHD (anginal attacks), but also marked stress-induced, myocardial perfusion defects.

Angina Pectoris↗
PubMed1998

The "warm-up" phenomenon occurs in patients with chronic stable angina but not in patients with syndrome X.

Most patients with chronic stable angina show an improvement in ischemic threshold when a second exercise test is performed a few minutes after a first positive test. In this study we evaluated whether this "warm-up" phenomenon also occurs in patients with syndrome X. We performed 2 consecutive exercise tests in 14 patients with chronic stable angina and 11 patients with syndrome X. The second exercise test was performed after 10 minutes from the end of the first one, always after complete recovery to baseline of ST segment. In patients with stable angina, heart rate (108+/-18 vs 99+/-16 beats/min, p = 0.005), rate-pressure product (17,020+/-4,541 vs 15,215+/-3,734 beats/min x mm Hg, p = 0.028), and exercise time (587+/-297 vs 444+/-244 seconds, p = 0.002) at 1-mm ST depression were higher in the second test than in the first one and a significant improvement in these parameters during the second test was also observed at peak exercise. Conversely, in patients with syndrome X, there were no significant differences between the 2 tests in heart rate (128+/-18 vs 131+/-23 beats/min), rate-pressure product (19,922+/-5,153 vs 19,390+/-5,654 beats/min x mm Hg), and exercise time (592+/-243 vs 566+/-228 seconds) at 1-mm ST-segment depression. Similarly, in this group of patients, no significant differences in exercise variables between the 2 tests were observed at peak exercise. Thus, unlike patients with chronic stable angina, patients with syndrome X have no evidence of warm-up in response to repeated exercise testing.

Adaptation, Physiological↗
PubMed2002

Central neural contribution to the perception of chest pain in cardiac syndrome X.

OBJECTIVE: To investigate the central neural contribution to chest pain perception in cardiac syndrome X (angina-like pain, ECG changes during stress, angiographically normal coronary arteriogram). SUBJECTS: Eight syndrome X patients and eight healthy volunteers. METHODS: Dobutamine stress using echocardiography to assess myocardial function, and positron emission tomography to measure changes in regional cerebral blood flow, as an index of neuronal activity. RESULTS: During similar doses of dobutamine, syndrome X patients and controls showed comparable regional cerebral blood flow changes in the hypothalamus, thalami, right orbito-frontal cortex, and anterior temporal poles, associated with the sensation of a fast or powerful heart beat. In patients, but not controls, the stress also generated severe chest pain associated with increased activity in the right anterior insula/frontal operculum junction. There were ischaemia-like ECG changes in the syndrome X patients, but no left ventricular dysfunction on echocardiography. Activation of the right insula during chest pain clearly distinguished the syndrome X patients from a group of patients with known coronary disease. CONCLUSIONS: Chest pain and ECG changes were not accompanied by demonstrable myocardial dysfunction in syndrome X patients, but altered central neural handling of afferent signals may contribute to the abnormal pain perception in these patients.

Aged↗
PubMedDate not supplied

A sustained release formulation of isosorbide-5-mononitrate with a rapid onset of action.

The clinical efficacy of a combined immediate-release and sustained-release preparation of isosorbide-5-mononitrate for angina pectoris is observed within a few minutes of administration. The preparation reduces the number of silent and painful ischaemic episodes and increases work and exercise capacity. The pharmacokinetic profiles accord with the circadian variation in cardiovascular disease. Drug levels fall significantly at night and tolerance to the haemodynamic and antianginal effects is not seen. Once-daily administration is appreciated by patients. The preparation also shows promise in treating heart failure.

Angina Pectoris↗
PubMed1993

[The role of the vascular endothelium and vasospasm in different coronary syndromes. A common physiopathological base for distinct entities?].

A literature review on the endothelial functions and endothelial dysfunction/lesion, as well as the atherosclerosis role in this process is performed. The several physiological explanations of both acute and chronic coronary syndromes are also reviewed, with particular emphasis to the recent studies on vasospasm mechanisms and its role in the physiopathogeny of variant angina and syndrome X. The role of the endothelial dysfunction/lesion as a common physiopathological basis to all coronary syndromes, is discussed.

Angina Pectoris, Variant↗
PubMed2005

Angina pectoris with a normal coronary angiogram.

Angina in the setting of a normal angiogram (NOCAD) occurs in 20-30% of patients undergoing coronary angiography. The etiologies of NOCAD can be anatomically classified into three groups: epicardial disease, coronary microvascular dysfunction, and noncoronary disease. Epicardial disease resulting in NOCAD includes endothelial dysfunction, coronary artery spasm, and coronary artery bridging. Microvascular dysfunction may be secondary to hypertension, cardiomyopathy, infiltrative disease, valvular disease, or idiopathic. Noncoronary artery disease states involving other organs systems such as the pulmonary, gastrointestinal, or musculoskeletal systems can also result in NOCAD. This review focuses on the coronary etiologies of NOCAD. The pathophysiology of disease is discussed as well as a systematic diagnostic strategy. Potential therapeutic options and prognosis are also reviewed.

Clinical Trials as Topic↗
PubMed1996

Value of intracoronary ultrasound and Doppler in the differentiation of angiographically normal coronary arteries: a prospective study in patients with angina pectoris.

BACKGROUND: A substantial proportion of patients undergoing heart catheterization for suspected coronary artery disease have normal angiograms. Coronary morphology and blood flow velocity can be assessed very accurately with intracoronary ultrasound and Doppler. The purpose of this study was to use both methods to classify further patients with suspected coronary artery disease but with coronary angiograms adjudged normal at the time. METHODS AND RESULTS: In forty-four patients with suspected coronary artery disease and normal coronary angiograms, intracoronary ultrasound and intracoronary Doppler were performed in the left anterior descending and left main coronary arteries. Coronary flow reserve was obtained by calculating the ratio of the maximal coronary flow mean velocity after the intracoronary administration of 10 mg papaverine to the coronary flow mean velocity at rest. Of 44 patients, 16 (36%) (group I) were found to have normal coronary morphology by intracoronary ultrasound and normal (> 3.0) coronary flow reserve (5.3 +/- 1.8). In seven patients (16%) (group II) there were normal intracoronary ultrasonic findings but a reduced coronary flow reserve (2.1 +/- 0.4). Plaque formation was found in a total of 21 (48%) of the 44 patients; mean plaque sizes were 3.6 +/- 1.6 mm2 for those in group III (normal coronary flow reserve) and 5.0 +/- 2.3 mm2 for those in group IV (reduced coronary flow reserve). Vessel area in both of these groups (16.3 +/- 8.0 mm2 and 19.2 +/- 6.1 mm2) was significantly larger than that of group I (14.6 +/- 5.7 mm2, P < 0.01). Plaque calcification was found in 25% of those in group III and 44% of those in group IV. Thus, only 36% of the patients with normal angiograms were true normal, 48% exhibited early stage of coronary atherosclerosis, and the other 16% might be considered as syndrome X. CONCLUSION: Intracoronary ultrasound and Doppler can be used to differentiate further heart disease in patients with normal coronary angiograms. Only a minority were true normal. Early signs of atherosclerosis cannot be detected by coronary angiography. This may have important therapeutic and prognostic implications.

Adult↗
PubMed1993

Clinical presentation and functional prognosis in syndrome X.

OBJECTIVES: To assess the effect of clinical presentation on functional prognosis in patients with syndrome X. DESIGN: A prospective study. Patients with syndrome X presenting with unstable angina and stable angina were followed up with a questionnaire to examine their functional state. PATIENTS: 41 patients with syndrome X and unstable angina and 41 patients with syndrome X and stable angina. Syndrome X was defined as typical anginal chest pain, a positive exercise test, and normal coronary angiogram. SETTING: Regional cardiothoracic centre. RESULTS: The mean follow up time was 36 (range 20-51) months for the unstable angina group and 35 (range 19-51) months for the stable angina group. No patient was lost to follow up in either group. At follow up 28 patients in the unstable angina group were pain free compared with 15 patients in the stable angina group (p = 0.008). Seven patients in the unstable angina group had further hospital admission with chest pain after the cardiac catheterisation compared wtih 12 patients in the stable angina group (NS). Seven patients in the unstable angina group believed that they had heart disease compared with 27 in the stable angina group (p < 0.001). 26 patients in the unstable angina group but only eight patients in the stable angina group were unlimited in their physical activity (p < 0.001). 12 patients in the unstable angina group compared with 27 patients in the stable angina group were unable to work normally because of chest pain (p < 0.001). The mean (SD) duration of symptoms before cardiac catheterisation was 7.9 (4.7) months in the unstable angina group and 13.4 (5.6) months in the stable angina group (p < 0.001). 10 patients in the unstable angina group and 24 patients in the stable angina group still attended hospital outpatient clinics because of chest pain (p = 0.004). 16 patients in the unstable angina group and 29 patients in the stable angina group were still taking regular antianginal medication (p < 0.001). CONCLUSIONS: Patients with syndrome X who present with unstable angina have a significantly better functional prognosis than those presenting with symptoms of stable angina. This may reflect differences in underlying pathophysiological mechanisms.

Adult↗