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At least 1,369 records · Page 76Linked to original sources
PubMed1990

Panic disorder in cardiology patients.

This paper reviews current evidence from several cardiology populations that suggests panic disorder is prevalent and underdiagnosed. Cardiology patients with atypical angina and no heart disease have a high likelihood of having panic disorder as suggested by studies of two separate cardiology populations. That they resemble psychiatric populations with panic is suggested by their positive response to alprazolam. Although evidence is less clear concerning the relationship between MVP and panic, it appears that patients referred to ECHO and found to have MVP are also likely to have panic. Three other populations deserving further study are patients with 1) pacemaker syndrome, 2) coronary artery disease with atypical angina and 3) certain arrhythmias.

Adult↗
PubMedDate not supplied

[Surgical treatment of Prinzmetal's syndrome. Report of sixty operated cases (author's transl)].

The results of the surgical treatment of Prinzmetal's angina are reported in this study of 60 patients. The operative mortality is 3,3 percent and the incidence of post-operative infarction is 20 percent. 53 patients were followed over an average period of 2,7 years. The global survival rate is 91 percent at 5 years, the infarction rate is 24 percent. 76 percent of the sublims are asymptomac. The patients can be classified in three group : isolated lesions, multiple lesions and spasms.

Angina Pectoris↗
PubMedDate not supplied

[Coronary spasm during exercise test (author's transl)].

We thought chest pain associated with ST segment elevation during exercise test in patients with not significant coronary lesions could be related to coronary spasm. Three patients with mild coronary obstructive lesions underwent coronary arteriography during exercise test. In two patients this hypotesis was supported by angiographic documentation of the coronary spasm.

Angina Pectoris↗
PubMed1990

[ST-T segment alternans in ventricular tachycardia associated with inversion of the U wave in Prinzmetal angina during exercise test. Description of a clinical case].

A case of ST segment alternans during effort angina is described. This is the seventh such case in the literature. Here the alternans appeared during a ventricular tachycardia. As with the other cases in literature, the alternans took place during an ischemic attack which affected the anterior wall.

Angina Pectoris, Variant↗
PubMed1989

[Activation and inhibition of adrenergic effects on the coronary vessels of patients with different forms of angina pectoris].

Experimental data in animals indicate that coronary vasoconstriction occurs following blockade of the beta-adrenergic receptors or alpha-receptors activation. The vasomotor effects of these maneuvers in man are unclear. Therefore we investigated whether and to which extent alpha-stimulation (cold pressor test: CPT) and beta-blockade (propranolol) cause coronary vasoconstriction; whether this effect involves the resistance arterioles as well as the large epicardial branches, and, within these, whether the normal and stenotic tracts are involved. Patterns in patients with effort angina were compared with those in patients with Prinzmetal angina. We studied 19 cases with classic and 15 cases with Prinzmetal angina. The systemic, pulmonary and coronary hemodynamics (pressure, flow and resistance) and the vasomotor pattern of normal and stenotic epicardial branches (quantitative angiography) were evaluated in the baseline condition, during CPT, after propranolol (5 mg iv) and during CPT repeated after propranolol. We observed that: changes of the coronary flow due to beta-blockade and to CPT are related to the variations of the myocardial oxygen consumption, induced by the inhibition and activation of adrenergic receptors and not to the concomitant vasomotor reaction of the stenotic vascular tract; beta-blockade does not affect homogeneously the lumen of the stenotic lesions in effort angina and invariably increases the lumen in the Prinzmetal form; influences of CPT, in the absence as well as in the presence of beta-receptor blockade, on the lumen diameter of both normal vessels and stenotic lesions are minimal in either form of angina.

Angina Pectoris↗
PubMed1989

[Determining the vasospastic origin of stenocardia attacks on the basis of 24-hour ECG monitoring].

The pattern of anginal attacks was evaluated, using 24-hour ECG monitoring, in 67 patients with angina at rest, as compared to 60 patients with angina of effort. In most patients, ischemic ECG changes developed in the presence of unchanged heart rate at rest or heart rate increment of less than 0.25 of the daily peak, and disappeared as heart rate increased. A U-like pattern of ST displacement was noted. These features were found to be typical for the vasospastic mechanism of anginal attacks developing at rest. Therefore, the origin of anginal attacks can be identified by means of ECG monitoring.

Adult↗
PubMed1989

[Spastic angina].

The article reports a case of vasospastic angina. The disease is caused by a spasm in a large epicardial coronary artery which may otherwise be normal or show variable degrees of atherosclerosis. The diagnosis must be differentiated from acute myocardial infarction, unstable angina of arteriosclerotic origin and extracardial diseases. ECG may show transient elevation of the ST-segments and coronary arteriography can directly visualize the spasm during a spontaneous attack. Aggressive therapy with calcium antagonists and long-acting nitrates often has an excellent symptomatic effect and may improve the prognosis.

Aged↗
PubMed1989

[Comparison of the coronary vasomotor response to nifedipine in syndrome X and in Prinzmetal's angina].

In this study we tested whether Ca++ has a similar part in the coronary vasomotion of patients with syndrome X (n = 29) and patients with Prinzmetal angina pectoris (n = 12). Through quantitative angiography we evaluated the influence of nifedipine (10 mg sl) on the lumen diameter of proximal, mid and distal thirds of normal epicardial branches. The main differences in the coronary vasomotor reaction were: uniform vasodilatation in Prinzmetal angina and a variable response in syndrome X; greater increase in the coronary lumen in patients in the former as compared to those in the latter group who showed vasodilatation. The variable response in syndrome X was not related to changes in diastolic pressure and cardiac output. Patients showing coronary constriction were those who responded to nifedipine with a higher degree of tachycardia; this might suggest a neural participation in the paradoxical reaction to this drug. In the Prinzmetal group, on the contrary, at similar heart rate increase the pattern was invariably vasodilatation. Thus, calcium ions appear to have a different role in the coronary smooth muscle contractility of the 2 series of patients; in fact, in Prinzmetal angina nifedipine relaxed the coronary arteries more potently and made them unresponsive to stimuli which were still able to cause vasoconstriction in syndrome X.

Adult↗
PubMed1985

[Transmural myocardial infarction and Prinzmetal's syndrome in an allergic reaction to glafenine. Physiopathological discussion. Apropos of a case].

The authors report the case of a 38 year old man who experienced at two month' interval, hypersensitivity reactions to the ingestion of 200 mg tablets of glafenine, complicated on the first occasion by a transmural anterior wall myocardial infarction as the first manifestation of coronary artery disease and on the second occasion by Prinzmetal angina due to posterior wall ischaemia. Coronary angiography was more or less normal. The timing of the symptoms in the context of an anaphylactic reaction and their repetition when the same molecule was reintroduced are strong arguments in favour of the pathogenic role of glafenine, even in the absence of biological criteria which are always variable. The mechanism of the coronary problems is discussed with reference to mediators released during the anaphylactic reaction: coronary vasoconstriction due to histamine and leukotriene release; inhibition of prostaglandin synthesis causing potentiation of the effects of histamine; lowering of the vasodilatory and antiaggregant prostacyclin enhancing the vasoconstrictor and platelet aggregant action of thromboxane A2. All the conditions favouring the initiation of coronary spasm with eventual coronary thrombosis, the one aggravating the other, are therefore present.

Adult↗