1/25. Recurrent syncopal episodes of neurocardiogenic origin in a patient suffering from cardiac syndrome-X. We describe the case of a 44-year-old man, with a history of recurrent syncopal episodes and effort angina, the latter attributed to cardiac syndrome-X, who was admitted to our department because of a syncopal episode. During his hospitalization laboratory investigations including haematologic and blood chemical findings, head C/T scan, electroencephalogram, 48-hour Holter monitoring, electrophysiologic testing and echocardiographic study disclosed no abnormalities. On the contrary, a passive upright tilt testing was found to be positive, resulting, approximately, in a 10-seconds time interval of asystole accompanied by syncope. The association in the same patient of cardiac syndrome-X and neurocardiogenic syncope, although never described before, might be explained by a similar pathophysiological mechanism, which is a sympathovagal imbalance. ( info) |
2/25. A 42-year-old man with recurrent myocardial infarction and normal appearing coronary arteries. We report the occurrence of a coronary mural thrombus and recurrent myocardial infarction in a patient with normal-appearing epicardial coronary arteries and small-vessel coronary artery disease. The current case emphasizes the importance of permanent medical treatment with anti-platelet and vasodilators in patients with small-vessel coronary artery disease. ( info) |
| In patients with pseudoxanthoma elasticum, severe organic coronary artery stenosis often occurs without coronary risk factors. However, this report presents the case of a 49-year-old woman with pseudoxanthoma elasticum who had coronary artery spasm with an angiographically normal coronary artery. In addition, coronary artery spasm was provoked with dipyridamole thallium-201 cardiac imaging. ( info) |
| chest pain with normal coronary angiograms is a relatively common syndrome. The mode of presentation of this syndrome includes patients with syndrome X and patients with an acute myocardial infarction and angiographically normal coronary arteries. Different mechanisms have been proposed to elucidate the exact cause and to explain the various clinical presentations in these patients. Abnormalities of pain perception and the presence of oesophageal dysmotility have all been reported in patients with syndrome X. In situ thrombosis or embolization with subsequent clot lysis and recanalization, coronary artery spasm, cocaine abuse, and viral myocarditis have been described as potential mechanisms responsible for an acute myocardial infarction in patients with angiographically normal coronary arteries. Recent data suggest that both microvascular and epicardial endothelial dysfunction may play an important role in the pathophysiological mechanism of the syndrome of stable angina or acute myocardial infarction with normal coronary arteries. ( info) |
5/25. Enhanced platelet aggregation, high homocysteine level, and microvascular disease in diabetic muscle infarctions: implications for therapy. Muscle infarction is a rare complication in patients with diabetes mellitus, probably because of the rich vascular supply of this tissue. We describe a patient with type 1 diabetes who had infarction of the muscles in her right thigh. We report, for the first time, that the patient, in addition to an advanced microvascular disease in the muscle, had increased plasma total homocysteine levels and increased platelet aggregation. These pathologies might have a synergistic effect on the development of this rare complication and should be treated aggressively to prevent further episodes. ( info) |
6/25. Alteration of coronary flow velocity during spontaneous angina in a patient with microvascular angina. Phasic coronary flow velocity in the left and right coronary artery was recorded in a patient with microvascular angina. Coronary flow velocity during anginal attack was characterized by diminished systolic forward velocity, the appearance of systolic flow reversal, increase in diastolic flow velocity and its rapid deceleration. It was also accompanied with abnormal coronary flow reserve. These findings completely recovered at follow-up examination. A subgroup of patients with microvascular angina may show unique and reversible coronary flow abnormalities during chest pain. ( info) |
7/25. Case 1. Cardiovascular dysfunction syndrome. A 56-year-old woman is referred with angina. A number of sequential management strategies have been attempted with varying results. Upon examination of her case, it is clear that she has cardiovascular dysmetabolic syndrome and is thus at high risk for adverse cardiovascular events. Two opinions for further management are presented. ( info) |
| We report a 48-year-old woman with foregut ischemia with splenic infarct due to isolated celiac artery obstruction. The patient presented with acute-onset pain in the epigastrium 10-15 min after every meal. Investigations revealed obstruction of the celiac artery by artheromatous plaque. This patient had an acute thrombosis, which responded to anticoagulation. ( info) |
9/25. Resolution of syndrome X after eradication of virulent CagA-positive helicobacter pylori. A 42-year-old man with chest pain was found to have ST depression in leads V1 through V4. The coronary arteries appeared normal on angiography. Positive results of ventricular pacing and acetylcholine test led to a diagnosis of syndrome X. Other studies revealed gastritis due to CagA-positive helicobacter pylori. Classic therapy for angina did not resolve chest pain, but eradication of H. pylori led to disappearance of symptoms and negative test results. ( info) |
10/25. 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. ( info) |