Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Factors precipitating nocturnal myocardial ischaemia were investigated in 10 patients with frequent daytime and nocturnal angina pectoris. Eight patients had fixed obstructive coronary artery disease or a low exercise threshold or both before the onset of ischaemia. Two patients had variant angina with normal coronary arteries and negative exercise tests. During sleep the electrocardiogram, electroencephalogram, electro-oculogram, electromyogram, chest wall movements, nasal airflow, and oxygen saturation were continuously measured. Forty two episodes of transient ST segment depression were recorded in the eight patients with coronary artery disease and 26 episodes of ST segment depression and elevation in the two patients with variant angina and normal coronary arteries. All episodes of ST segment depression in the former group of patients were preceded by an increase in heart rate as a result of arousal and lightening of sleep, bodily movements, rapid eye movement sleep, or sleep apnoea (one episode). In contrast, in the variant angina group no increase in heart rate, arousal, or apnoea preceded 23 of the 26 episodes of ST segment change. Thus increase in myocardial oxygen demand was important in precipitating nocturnal angina in patients with coronary artery disease and reduced coronary reserve. In the patients with coronary spasm these factors did not often precede the onset of nocturnal myocardial ischaemia.
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PMID:Nocturnal angina: precipitating factors in patients with coronary artery disease and those with variant angina. 376 13

We injected acetylcholine (ACh), the neurotransmitter of the parasympathetic nervous system, into the coronary arteries of 28 patients with variant angina. Injection of 10 to 80 micrograms ACh into the coronary artery responsible for the attack induced spasm together with chest pain and ST segment elevation or depression on the electrocardiogram in 30 of the 32 arteries of the 25 of the 27 patients. The injection of 20 to 100 micrograms ACh into the coronary artery not responsible for the attack in 18 patients resulted in various degrees of constriction in most of them, but no spasm in any of them. After intravenous injection of 1.0 to 1.5 mg atropine sulfate, the injection of ACh into the coronary artery responsible for the attack did not induce spasm or attack in any of the nine coronary arteries injected in eight patients. We conclude that the intracoronary injection of ACh induces coronary spasm and attack in patients with variant angina and that the activity of the parasympathetic nervous system may play a role in the pathogenesis of coronary spasm. We also conclude that the intracoronary injection of ACh is a useful test for provocation of coronary spasm.
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PMID:Induction of coronary artery spasm by acetylcholine in patients with variant angina: possible role of the parasympathetic nervous system in the pathogenesis of coronary artery spasm. 376 79

A patient with significant left anterior descending coronary disease is presented who developed significant ST segment elevation and depression at different times under similar testing conditions. Currently proposed explanations for exercise-induced ST segment elevation are discussed. This patient likely represents a case of spasm superimposed on significant obstructive disease, so-called mixed angina.
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PMID:Exercise-induced ST-segment depression and elevation in the same patient. A case for mixed angina. 376 87

Nineteen patients with syndrome X (typical exertional angina, positive exercise test response [at least 0.1 mV of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries) underwent continuous 48-hour electrocardiographic (ECG) monitoring during unrestricted daily life. Fifty-eight ischemic episodes of at least 0.1 mV of ST-segment depression were observed in the same ECG leads that showed ST depression during stress testing: 28 (48%) were accompanied by anginal pain and 30 (52%) were asymptomatic. No significant differences were found between painful and silent ST-segment depression with regard to the number of episodes, their temporal distribution, magnitude, duration or heart rate (HR) at onset of ST-segment depression. In the minute preceding ischemic ST shifts, HR did not change in 33% of episodes or increased by less than 10 beats/min in 28%. HR at onset of ST depression was significantly lower during ambulatory ECG monitoring than during exercise testing (98 +/- 18 vs 117 +/- 18 beats/min, p less than 0.01). During ambulatory monitoring, 85 episodes of sinus tachycardia (exceeding by 10 to 80 beats/min the HR that triggered ischemia during exercise testing) occurred in the absence of angina or ST-segment shifts. The results of this study suggest that in patients with syndrome X, myocardial ischemia frequently develops during daily life; silent ischemia is an important component of this syndrome; and increased oxygen demand in the presence of impaired coronary vasodilatory capacity is not the only cause of myocardial ischemia. Active mechanisms that transiently reduce coronary flow may act and explain occurrence of angina at rest and with minimal exertion.
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PMID:Transient myocardial ischemia during daily life in patients with syndrome X. 378 14

This study was performed to determine the sensitivity of thallium imaging vs ECG monitoring for detecting coronary artery spasm noninvasively following intravenous ergonovine administration as compared to simultaneous coronary angiography. Thirty-two patients with insignificant coronary artery disease and chest pain underwent 12-lead ECG monitoring, thallium imaging, and coronary arteriography following the administration of 0.05, 0.1, 0.2, and 0.3 mg of ergonovine given 5 minutes apart or until chest pain occurred. One minute following the last dose of ergonovine, 2.5 mCi of thallium-201 was injected intravenously, and a final ECG was recorded and repeat coronary arteriography performed. Within 10 minutes following the injection of thallium, imaging was performed in the 40-degree and 70-degree left anterior oblique and anterior projections. The ECG, thallium study, and coronary arteriogram were read blindly and results were compared. The ECG, angiogram, and thallium study were read as positive if the following occurred, respectively: greater than or equal to 1 mm ST segment elevation, depression, or T wave reversal; greater than 50% vessel narrowing,; and reversible perfusion defect. Five patients were excluded from analysis because of either catheter-induced spasm, suboptimal thallium studies, or protocol violations. Of the 27 patients included for analysis, six had chest pain, five had a positive angiogram, five had a positive thallium study, and one had a positive ECG. The sensitivity of thallium vs ECG monitoring was 80% vs 25%, and the accuracy was 92% vs 80%. We conclude that thallium imaging greatly increases the noninvasive detection of ergonovine-induced coronary spasm as compared with the ECG with no loss of accuracy.
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PMID:Comparison of electrocardiography and thallium-201 myocardial scintigraphy for the detection of ergonovine-induced coronary artery spasm: angiographic correlation. 382 55

Regional myocardial blood flow during exercise was determined using the thermodilution technique in 2 patients suffering from both spontaneous and exertional chest pain. In both cases we observed that effort-related anginal attacks were due to coronary spasm with sudden reduction of regional left ventricular blood flow. In 1 patient the exercise-induced ST-segment elevation in the anterior leads was accompanied by a reduction of flow in the great cardiac vein. In the second patient the exercise-induced ST-segment depression in the lateral leads was accompanied by a reduction of coronary flow in the area supplied by the circumflex artery. In 1 patient, nifedipine was effective in prolonging exercise tolerance by preventing the occurrence of coronary spasm and by increasing blood supply to the ischemic region during exercise.
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PMID:Exercise-induced coronary artery spasm. A regional coronary blood flow study. 383 6

The frequency and magnitude of objectively determined myocardial ischaemia during normal daily activities of patients with varying severity of coronary artery disease are unknown. Furthermore, the incidence of nocturnal resting myocardial ischaemia and frequency of coronary spasm in patients with normal coronary arteries and chest pain are also not known. One hundred consecutive patients with chest pain referred for coronary angiography were therefore investigated with exercise testing and ambulatory ST segment monitoring. Fifty two of 74 patients with significant coronary artery disease and six of 26 with no significant coronary narrowing had episodes of ST segment change during 48 hours of ambulatory monitoring. Two patients, one with normal coronary arteries and localised spasm and one with three vessel disease, had episodes of ST segment elevation, whereas all other patients had episodes of ST segment depression. The frequency, duration, and magnitude of ST segment changes were greater in patients with more severe types of coronary artery disease. Thus more than six episodes of ST segment change per day occurred in patients with two or three vessel disease or left main stem stenosis and in the only patient with coronary spasm and normal coronary arteries. Nocturnal ischaemia occurred in 15% of patients with coronary artery disease and was almost an invariable indicator of two or three vessel coronary artery disease or left main stem stenosis. Episodes of ST segment change occurred most commonly during the morning hours and least commonly during the night, in parallel with changes in basal hourly heart rates. The heart rate at the onset of ST segment change tended to be lower in patients with coronary artery disease than in those with normal coronary arteries. The duration of exercise to ST segment depression tended to be shorter in patients with more severe disease, but it could not predict patients with nocturnal myocardial ischaemia, left main stem stenosis, or coronary spasm, whereas ambulatory ST segment monitoring was able to identify most of these patients.
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PMID:Morphology of ambulatory ST segment changes in patients with varying severity of coronary artery disease. Investigation of the frequency of nocturnal ischaemia and coronary spasm. 396 60

We studied the clinical characteristics of 153 patients with angina pectoris associated with coronary artery spasm (CAS). The study was designed to investigate the relationship of CAS to ST segment deviation and to the site of fixed stenosis, and hemodynamic alteration during a spastic event. Analysis of coronary arteriograms and multilead electrocardiograms obtained simultaneously from 170 events of CAS by the use of radioluscent carbon-fiber electrodes resulted in 58 events with ST elevation which were related to total occlusion of major coronary arteries due to CAS; another 54 events with ST depression, in which the affected coronary arteries demonstrated severe but incomplete occlusion, or total occlusion but were visualized via collateral vessels; and remaining 58 events without ST deviation showing mild occlusion. The results indicate a close correlation between magnitude of CAS and ST segment deviation. CAS occurred at the site of pre-existing fixed stenosis including minor plaque defect in 133 patients and at apparently normal site in 20 patients. In the former group, only four patients had triple vessel disease, while 95 had nonsignificant fixed lesion. In the latter group, 10 patients had minor lesion distant from the site of CAS. Thus, CAS is closely related to fixed stenosis, which may have but a limited role as a cause of CAS. Hemodynamic measurements during spastic events were obtained from 49 patients including 41 events with spasm of the left anterior descending artery (LAD) and 21 events with spasm of the right coronary artery (RCA). The onset of an increase in left ventricular (LV) filling pressure and a reduction in LV dP/dt preceded ST segment deviation in all events. The first hemodynamic variable manifested in the spastic event was the reduction of LV contraction dP/dt in the majority of patients. The increase of LV filling pressure was greater in LAD spasm than RCA spasm (11 +/- 6 mmHg vs 7 +/- 4 mmHg, P less than 0.0125) and in events with ST elevation than with ST depression (11 +/- 5 mmHg vs 6 +/- 5 mmHg, p less than 0.001). Right ventricular functional impairment was mild in most patients during CAS. The study indicates that mechanical impairment precedes electrical impairment during CAS and that LAD spasm with ST elevation represents the most severe LV dysfunction.
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PMID:Clinical characteristics of coronary artery spasm: electrocardiographic, hemodynamic and arteriographic assessment. 396 65

Since hypercholesterolemia sensitizes isolated rabbit coronary arteries to vasoconstrictor stimuli, we assessed the possibility of reproducing occlusive coronary spasm both in vitro and in vivo in atherosclerotic rabbits. In Langendorff-perfused hearts from nine atherosclerotic rabbits (2% cholesterol diet for 18 weeks), despite a threefold increase of cholesterol concentration in the coronary wall compared with nine control rabbits, ergonovine and serotonin did not produce any increase of coronary vascular resistances; the increase produced by pitressin was significantly less in atherosclerotic than in normal hearts (56 +/- 13% vs 138 +/- 28%, p less than 0.05, respectively), whereas that produced by phenylephrine was similar (10.1 +/- 1.8% vs 8.5 +/- 2.4%, p = n.s.). In eight other unanesthetized rabbits we recorded the ECG during ergonovine administration (0.05 mg/kg) and during hypothalamic stimulation before and at regular intervals during the 2% cholesterol diet; rabbits survived for periods ranging from 1 to 22 weeks (mean 9.6 weeks). Only one animal had ST depression during episodes of marked tachycardia; no ischemic ECG changes were ever observed in the other rabbits despite the diffuse subintimal coronary deposition of cholesterol found postmortem. Thus, in atherosclerotic rabbits with chronic marked hypercholesterolemia, coronary arteries do not develop occlusive coronary spasm as observed in patients with variant angina.
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PMID:Failure of experimental atherosclerosis to sensitize coronary arteries to spasm in hypercholesterolemic rabbits. 397 75

Angiographic and electrocardiographic manifestations of initial coronary air embolism were seen in 4 patients and in a dog. All 4 patients had angina pectoris, 2 had ST elevation, 1 patient had ST depression and 1 had no electrocardiographic change after the air embolus. Although the initial diagnosis in these 4 patients was coronary artery spasm, a subsequent ergonovine test response for coronary artery spasm was negative in the 3 patients in whom it was performed. In a dog, initial injection of air in a coronary artery produced ST-segment elevation and delayed clearance of contrast material. The angiographic appearance of initial air embolus was similar in the 4 patients and in the dog. The leading edge of contrast material that followed an air embolus stopped abruptly, appeared hazy and blunt, and pulsated back and forth. The air embolus produced temporary cessation of flow in the main artery and its branches. Initial injection of air during coronary arteriography mimics coronary artery spasm by producing a syndrome characterized by angina, ischemic changes on the electrocardiogram, and delayed flow of contrast material. An initial air embolus may be differentiated from true coronary spasm by several distinctive angiographic features.
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PMID:Initial coronary air embolus in the differential diagnosis of coronary artery spasm. 397 7


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