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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possibility that DL-carnitine has a protective effect during myocardial ischemia was evaluated by performing two rapid coronary sinus pacing studies 15 minutes apart in 21 patients with coronary artery disease. Eleven patients received DL-carnitine (20 or 40 mg/kg) before the second pacing study. The treated group had a significant increase in mean heart rate (12.5 beats/min, P less than 0.001), pressure-rate product (1,912 units, P less than 0.01) and pacing duration (3.2 minutes, P less than 0.001) after the administration of carnitine. The treated group also had improvements in percent myocardial lactate extraction (8.8 percent increase, P less than 0.001) and left ventricular end-diastolic pressure (a decrease of 5.3 mm Hg, P less than 0.05). There was significantly less S-T segment depression during the second pacing period in both the untreated and treated groups. The results of this study suggest that in ischemic human hearts with reasonably well preserved left ventricular function, DL-carnitine may improve the tolerance for stress associated with an increase in heart rate and pressure-rate product.
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PMID:Improved pacing tolerance of the ischemic human myocardium after administration of carnitine. 3 61

An anaesthetic technique comprising a combination of phenoperidine (0.1 mg . kg-1), diazepam (0.06 mg . kg-1) and pancuronium bromide (0.1 mg . kg-1) with controlled ventilation was evaluated in 12 patients with severe coronary artery disease. The heart rate, cardiac output and mean arterial blood pressure did not change significantly between the preinduction and postinduction measurements. The right atrial pressure and pulmonary capillary wedge pressure decreased significantly by 33% and 36%, respectively, probably due to the influence of positive-pressure ventilation. There was no depression of the left ventricular performance.
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PMID:Cardiovascular effects of neurolept anaesthesia in patients with coronary artery disease. 4 52

Serious arrhythmias are accepted to be the main cause of sudden death in acute coronary artery disease (CAD). The purpose of this study was to evaluate the frequency and type of cardiac arrhythmias in patients with chronic CAD. 67 patients with suspected chronic CAD, documented by history and/or Ecg-changes, were investigated by means of a dynamic Ecg (Holter Avionics) with an average of 11 hours monitoring. On the basis of concomitant ST-segment depressions the patients were divided into 3 groups (A: greater than 0.1mV; B: 0.05-0.09mV; C: less than 0.05mV). The frequency of serious arrhythmias increased significantly with a greater degree of ST-segment depression. Serious arrhythmias were observed in 54% in group A, in 46% in group B, but only in 24% in group C. The frequency of minor arrhythmias such as occasional (less than 12/min atrial or ventricular premature contractions was essentially the same in all 3 groups. In 12 patients more than one serious arrhythmia were documented. Of the serious arrhythmias observed, 94% were tachycardias and/or secondary to increased myocardial irritability and therefore could respond favourably to beta-blocking agents. We believe that arrhythmias in patients with known chronic CAD should be taken seriously and longterm treatment with beta-blockers considered.
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PMID:[Frequency and type of arrhythmias in patients with chronic coronary disease]. 5 24

Coronary haemodynamic and metabolic effects of propranolol and glyceryl trinitrate were studied in 12 patients with coronary artery disease and 5 without coronary heart disease, at rest and during tachycardia stress. Propranolol-associated reductions in indices of myocardial oxygen demand, left ventricle work, tension time, and left ventricle oxygen utilisation (LVVO2) were reversed when heart rate was controlled by atrial pacing. Adding glyceryl trinitrate at rest also restored heart rate but decreased the left ventricular work index and tension time index as coronary resistance declined paradoxically. Tachycardia-related increases in tension time index and LVVO2 were unchanged after propranolol, and ischaemia (angina, ST depression, and reduced lactate extraction) was not altered in most of the patients. During tachycardia, the addition of glyceryl trinitrate decreased the tension time index and LVVO2; angina recurred in only 4 patients, and ST depression and lactate extraction improved. Similar haemodynamic changes occurred in the patients with normal coronary arteries. In contrast with propranolol administered alone, propranolol plus glyceryl trinitrate enhances tachycardia tolerance and prevents tachycardia-induced manifestations of ischaemia. This action is attributed to glyceryl trinitrate-associated improvement in the adequacy of myocardial perfusion.
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PMID:Coronary and myocardial metabolic effects of combined glyceryl trinitrate and propranolol administration. Observations in patients with and without coronary disease. 10 30

Two hundred consecutive catheterized patients with unstable angina pectoris were reviewed to find clinical and noninvasive indicators of left main coronary artery disease (greater than or equal to 50% lesion). Thirty-five patients (17.5% of total) had left main coronary artery disease. There were no differences between patients with and without left main coronary artery disease in age, sex, results of resting electrocardiogram, congestive heart failure, dyspnea during pain, duration of longest pain, arrhythmias, response to medical therapy, or other risk factors. Crescendo angina pectoris (worsening of pre-existing angina), transient ST-segment depression with pain, simultaneous anterior and inferior ST changes during pain, and fluoroscopic calcification of the left main coronary artery were all significantly more common in patients with left main coronary artery disease. However, low sensitivity or low predictive value, or both, limit the usefulness of these clinical predictors. Left main coronary artery disease cannot be reliably predicted in patients with unstable angina pectoris before coronary arteriography.
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PMID:Clinical indicators of left main coronary artery disease in unstable angina. 15 94

The evaluation of angina pectoris in patients with idiopathic hypertrophic subaortic stenosis is difficult in those in the age group prone to coronary artery disease. Ten patients with angina pectoris, normal coronary angiograms and idiopathic hypertrophic subaortic stenosis were studied with thallium-201 myocardial imaging performed in conjunction with submaximal treadmill exercise testing. The resting electrocardiogram demonstrated left ventricular hypertrophy with S-T segment abnormalities in seven patients, thereby vitiating the further increase in S-T segment abnormalities that developed in these patients during exercise or in the postexercise period. Of the three patients with a normal resting electrocardiogram, one had significant exercise-induced S-T segment depression. Thallium-201 myocardial imaging revealed no significant perfusion defects in 9 of the 10 patients (90 percent). In one patient with severe left ventricular hypertrophy significant perfusion defects developed after exercise that were not present at rest. Stress thallium-201 myocardial perfusion imaging is a useful noninvasive technique that assists in ruling out the presence of significant coronary artery disease in patients with idiopathic hypertrophic subaortic stenosis.
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PMID:Idiopathic hypertrophic subaortic stenosis: evaluation of anginal symptoms with thallium-201 myocardial imaging. 15 76

Electrocardiographic and cardiovascular responses during maximal exercise were evaluated in 103 normal children and in 82 children with familial hyperlipoproteinemia. The normal and hyperlipidemic children were comparable in regards to age, weight--height index, resting and exercise blood pressures, and maximal working capacity indices. The cohort of 82 hyperlipidemic children included 61 children (29 boys and 32 girls) with well defined "monogenic" familial hyperlipoproteinemia. Segmental ST depression on the exercise electrocardiogram occurred in 8 of these 29 boys (27.6%) as compared to 4 of 55 normal boys (7.3%), P less than 0.025 and in 6 of the 32 girls (19%) as compared to 7 of 48 normal girls (14.6%), P greater than 0.1. Segmental ST depression was present in 14 of 61 (23%) children with "monogenic" hyperlipoproteinemia, as compared to 11 of 103 (10.75%) normal (x2 = 4.47, P less than 0.05). An assessment of the clinical significance of an abnormal exercise electrocardiogram in male children with "monogenic" hyperlipoproteinemia must await the following: (1) two to four decades of observation and study of the development of morbid or mortal coronary disease, or (2) the future development of improved invasive or noninvasive techniques for the early detection of covert coronary occlusive disease. Currently, maximal exercise electrocardiography cannot be contemplated as a useful indicator of eventual premature coronary artery disease in asymptomatic hyperlipidemic children.
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PMID:Maximal exercise stress testing in normal and hyperlipidemic children. 18 80

An unexpected high incidence of false negative ST-segment responses to exercise was previously reported for patients with coronary artery disease and abnormal left-axis deviation on their resting electrocardiograms. In the case presented, an exercise-induced, "ischemia" ST-segment depression was masked with the onset of rate-dependent left-axis deviation. The state of the base-line electrocardiogram is an important but often overlooked factor in assessing the incidence of false negative and false positive ST-segment responses to exercise.
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PMID:Masking of exercise-induced ST-segment depression by rate-dependent left-axis deviation. 24 17

The alert physician can identify and probably alter the risk of sudden death for certain patients (see Table 5). It appears preferable to study the patient who has already been identified as having coronary artery disease because of clinical symptoms such as R/O MI, which has been shown to have a high risk for subsequent sudden death. In addition, the physician must be sensitive to the middle-aged man with multiple coronary artery disease risk factors who suddenly decides to have a routine check or develops nonspecific complaints. Once identified, patients can be educated to minimize delay time in seeking medical help with crescendo or prolonged angina. Ambulatory ECG monitoring for detection and characterization of ventricular arrhythmias, and exercise stress testing to detect severe ST depression, can facilitate an estimation of the patient's prognosis. A therapeutic plan, including attack on the patient's coronary artery disease risk factors, patient education, and specific medical or surgical therapies may alter the risk of sudden death. Once an infarction has occurred, rapid transport to a coronary care unit or monitoring facility, and administration of intramuscular lidocaine by medical or paramedical personnel when feasible, appear to lessen out-of-hospital mortality.
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PMID:Sudden death. 29 35

The effects of propranolol, digoxin and combination therapy (/D) on the resting and exercise ECG were studied in ten normal subjects and 20 patients with coronary artery disease (CAD) given a sequence of oral placebo, propranolol, P/D, digoxin and placebo, for two week periods. Digoxin produced a significant decrease in T-wave amplitude and often resulted in ST segment depression in the resting ECG. Propranolol, digoxin, and P/D tended to decrease the QTc interval and prolong the PR interval. However, CAD patients were more sensitive to PR prolongation than normals while receiving propranolol or digoxin alone. Propranolol therapy did not significantly affect the ST segment of the exercise ECG in the normal subjects or the CAD patients without an ischemic control exercise ECG. By contrast, 50 per cent of the normal subjects developed "false-positive" ischemic ST segment responses to exercise while receiving digoxin of P/D and three of eight CAD patients without ischemic control exercise ST segments had a similar response to digoxin or P/D. In 12 CAD patients with ischemic control exercise ST segments, propranolol did not affect the amount of ST segment depression at the onset of angina or the maximum amount of ST segment depression. Digoxin or P/D both uniformly increased the maximum amount of ST segment depression which was greater with digoxin than P/D. However, the maximum heart rate on P/D was significantly reduced as compared to that on digoxin. It is concluded that (1) CAD patients are more sensitive to propranolol or digoxin-induced AV block than normals, (2) propranolol does not change the magnitude of ischemic exercise ST segment depression, (3) digoxin increases ischemic exercise ST segment depression and results in a high incidence of false-positive exercise tests, and (4) the addition of propranolol to digoxin attenuates the effects of digoxin on the exercise ST segment.
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PMID:The effects of oral propranolol, digoxin and combination therapy on the resting and exercise electrocardiogram. 31 42


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