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)

Nifedipine, a slow-channel calcium blocker, is thought to provide useful myocardial protection during prolonged total ischemia and reperfusion. An isolated, isovolumic, feline heart model was used to asses the effectiveness of nifedipine in both cardioplegic (100 microgram/10 ml) and noncardioplegic (10 microgram/10 ml) doses for providing myocardial preservation during 90 minutes of hypothermic ischemic arrest and 45 minutes of normothermic reperfusion. Use of nifedipine was compared to hypothermia (27 degrees C) alone and to hypothermia with potassium cardioplegia. Ventricular function was assessed by recovery of isovolumic left ventricular developed pressure and dP/dt. Myocardial carbon dioxide tension (PCO2) and myocardial oxygen tension (PO2) were measured by mass spectrometry. Potassium cardioplegia and the higher dose of nifedipine resulted in immediate asystole. The rates of rise of PCO were greatest in the group receiving 10 microgram nifedipine and in the control group. The rates of rise in the two cardioplegic groups were significantly lower. Recovery of ventricular function was significantly lower with low-dose nifedipine than with potassium cardioplegia. Higher dose nifedipine resulted in a return of function, which was no different than with potassium cardioplegia. Morphologic protection was better with higher dose nifedipine and potassium cardioplegia than with either low-dose cardioplegia or hypothermia alone. These results demonstrate that nifedipine in a cardioplegic dose results in preservation of myocardial structure and function that is similar to that obtained with potassium cardioplegia. In lower noncardioplegic dose, nifedipine does not appear to offer additional protection compared to hypothermia alone. Whether persistent depression of ventricular contractility will limit nifedipine's clinical usefulness as a myocardial protection agent will require further study.
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PMID:Comparison of myocardial protection with nifedipine and potassium. 44 71

Reentrant ventricular arrhythmias (RVA) were analyzed in dogs 3--7 days after ligation of the anterior descending coronary artery using averaged "composite" recordings of electrical activity of reentrant pathways (RP) from the epicardial surface of the infarction zone (IZ). Verapamil (V) and D-600 (D) (0.2--0.5 mg/kg i.v.) resulted in slight-to-moderate improvement of conduction in RP with abolition of spontaneous RVA and RVA initiated by premature depolarizations. The effect of V was not blocked by pretreatment with propranolol (0.5 mg/kg i.v.). Using a standard microelectrode technique and strips of epicardial muscle from the IZ, D (0.5--1 X 10(-6) g/ml) slightly improved the upstroke velocity and membrane responses of depressed ischemic cells. In contrast, tetrodotoxin (5 X 10(-7) g/ml) further depressed or abolished action potentials of ischemic cells. We conclude: 1) the moderate antiarrhythmic effect of V and D on RVA is the result of improved conduction in RP; 2) this action is partly explained by improvement of a depressed sodium channel and is not related to catecholamine release; 3) slow-response action potentials play no significant role in the genesis of ischemia-related RVA, which probably results from depression of the fast response.
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PMID:Reentrant ventricular arrhythmias in the late myocardial infarction period. 7. Effect of verapamil and D-600 and the role of the "slow channel". 45 24

The effects of the beta-adernergic blocking drug acebutolol were studied in 23 patients with angina pectoris and angiographically documented coronary artery disease. Patients were evaluated clinically, by graded treadmill testing and by 24-hour Holter monitoring in the control state, after 2 weeks treatment with placebo, and after 2 weeks treatment with 600 mg. and then 1,200 mg. of acebutolol. Acebutolol (in a daily dose of 600 mg.) was an effective antianginal drug: the number of clinical attacks of angina pectoris (p less than 0.001) and the consumption of sublingual nitrate decreased (p less than 0.01), there was a significant increase in the treadmill effort tolerance as measured by the time to appearance of ischemic ECG changes (p less than 0.001) and the total work performed (p less than 0.001), and there was also a significant decrease in ischemic ST segment depression on 24-hour Holter monitoring. Treatment with 1,200 mg. acebutolol was associated with a further decrease in heart rate and a further improvement in effort tolerance on treadmill testing (p less than 0.05). On the large dose of the drug, however, there was no further clinical improvement, and no further improvement on 24-hour ECG monitoring; several patients complained of weakness and fatigue. Graded treadmill testing was an excellent objective method for assessing physical effort tolerance and its improvement after treatment with the beta-blocking drug. Twenty-four-hour Holter monitoring was a useful and complementary test, especially in patients who stopped exercising on the treadmill because of fatigue or weakness, and especially for assessing the efficacy of beta-blockade in controlling emotionally induced tachycardia and ischemia in the patient's own daily environment.
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PMID:Evaluation of the beta-blocking drug acebutolol in angina pectoris. 49 6

The purpose of this study was to determine the incidence of ST-segment depression during anesthesia and operation. Graded exercise testing has demonstrated a high correlation between ST-segment depression and myocardial ischemia. Therefore, 11 patients without and 29 patients with known coronary-artery disease were monitored during surgical procedures with a commercially available exercise electrocardiographic monitor (Viagraph). Comparisons were made between this device, which monitored lead V5, and the standard operating room monitor, which monitored lead 11. Eleven of 29 patients in the disease group demonstrated significant ST depression. Nine of the 11 ischemic episodes were not recognized on the standard operating room monitor. Retrospective review of anesthetic records of those 11 patients with ST-segment depression revealed rate--pressure product values greater than 11,000 for ten of them. Postoperatively, three of the 11 patients with significant ST-segment depression had changing electrocardiograms compatible with ischemia. None of the control group demonstrated significant ST-segment depression. The incidence of ischemia was 38 per cent during anesthesia and operation in the coronary-artery-disease group. Lead V5 analysis is superior to lead 11 analysis in detecting ST-segment depression. The period in which intubation is performed is one of the highest-risk intervals during anesthesia and operation, particularly when it is associated with an increased rate--pressure product.
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PMID:Myocardial ischemia during non-cardiac surgical procedures in patients with coronary-artery disease. 49 52

Hemodynamic monitoring and care of the patient at high risk for anesthesia require a careful and systematic approach. During preoperative evaluation the patient at increased risk must be identified and correctable problems must be solved. The patient's current medications must be reviewed because they may influence the choice of anesthetic approach and may alter the physiologic response to the stresses commonly associated with anesthesia. In addition to conventional clinical and electrocardiographic monitoring, perioperative hemodynamic monitoring may be desirable for patients at special risk, who are likely to have significant associated medical problems or to undergo complicated surgical procedures. No ideal induction agent exists, and hypotension secondary to peripheral vasodilation or myocardial depression, or both, is a potential problem. Patients with an inordinately high risk may benefit from mechanical circulatory assistance prior to induction of anesthesia. Attention to oxygenation, blood volume replacement and the prevention of hypertensive episodes are particularly important during anesthesia so that optimal cardiac performance is ensured and ischemia avoided. The stresses during emergence from anesthesia contribute to lability of the cardiovascular status and hypoxemia. The period of risk does not conclude with immediate recovery from anesthesia but extends through the postoperative phase. Careful monitoring and attention to the control of pain, prevention of hypotension and hypertension, adequate oxygenation, early mobilization and resumption of the administration of cardiac medications are important factors in a successful outcome.
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PMID:Hemodynamic monitoring and care of the patient of high risk for anesthesia. 49 83

Serial treadmill exercise testing (mean 5.5 tests/patient) was used to evaluate the prognosis of 200 males (mean age 53 years) without clinical heart failure or unstable angina pectoris 3 weeks after acute myocardial infarction (MI). Exercise-induced ischemic ST-segment depression greater than or equal to 0.2 mV 3 weeks after MI was significantly more prevalent in patients with subsequent cardiac arrest (100%) or coronary artery bypass graft surgery (64%) than in patients without subsequent events within 2 years of infarction (35%) (p less than 0.05). Exercise-induced ventricular arrhythmia on multiple tests 5-52 weeks after MI was more prevalent in patients with recurrent myocardial infarction (90%) than in patients without subsequent events (47%) (p less than 0.001). By contrast, exercise-induced ventricular arrhythmia on a single test at 3 weeks was a less powerful predictor of subsequent cardiac events. Exercise-induced ischemia 3 weeks after MI predicted early fatal events, while ventricular arrhythmia on serial testing predicted later nonfatal events.
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PMID:The prognostic significance of serial exercise testing after myocardial infarction. 49 48

Patients with chronotropic incompetence, defined as a failure of the heart rate response to exercise to rise to within two standard deviations of the expected increase with exercise, where studied and compared to patients with known coronary disease by angiogram with and without ST segment depression. 72% of the patients with chronotropic incompetence but without ST depression had significant coronary heart disease. The demonstration of chronotropic incompetence in exercise testing has important predictive implications and should be looked upon as carefully as ST segment changes. There was no evidence of SA node ischemia in these patients. Intrinsic heart rate measurements done in this study suggest autonomic dysfunction as a possible pathophysiologic mechanism for chronotropic incompetence. The heart rate response to exercise may be a useful predictor of the presence and severity of coronary disease. Therefore, a predicted heart rate response with standard deviation for age and sex should be included as part of the stress test protocol.
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PMID:Chronotropic incompetence in exercise testing. 49 1

The type of angina pectoris was determined in 47 women and 27 men aged 40 or less who then underwent quantitative left cineventriculography, coronary arteriography and atrial pacing test with determination of lactate concentrations from arterial and coronary sinus blood samples. The 29/74 patients with atypical angina and no narrowings on coronary arteriography (Group I) gave no pathological atrial pacing tests but 9 had pathological lactate tests. Group II consisted of 27/74 patients with typical angina but normal coronary arteriography. In these the atrial pacing test was pathological in 20 and the lactate test in 11. Coronary narrowings of 50% or more were found in 18/74 patients (Group III), who all had pathological pacing tests but only 9 pathological lactate tests. No statistical differences could be elicited between diagnostic groups in the quantitative evaluation of left ventricular function and it could be regarded as normal in 42/74 patients. The left ventricular mass index exceeded the control level in 6 patients in Group I and in 10 patients in Group II who all had a net lactate production upon pacing. The end-diastolic volume index was above control level in 11 patients in Group II, in whom the ST depression in pacing test was the only finding indicating ischemia. The hoop stress values exceeded the control level in both of these subgroups. In Group III 7 patients had a high left ventricular mass index and 4 a billowing mitral leaflet. The changes observed suggest disturbed functioning of left ventricle.
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PMID:Tests for ischaemia and left ventricular function in young patients with effort-induced chest pain. 51 93

We measured ventilatory responses to CO2 (delta VI/delta PCO2) and transient hypoxia (delta VI/delta SaO2) during reductions of brain blood flow (BBF) to 70% and 50% of control in unanesthetized goats. Increase in inspiratory volume per change in CO2 tension (delta VI/delta PCO2) was measured during rebreathing with sampling of both arterial and cerebral venous blood; increase in inspiratory volume per fall in arterial oxygen saturation (delta VI/delta SaO2) was assessed by the transient N2 inhalation method. Delta VI/delta SaO2 did not significantly change at 70% BBF, but was depressed at 50% BBF. Delta VI/delta PCO2 increased (0.94 +/- 0.18 to 1.29 +/- 0.24 l . min-1 . Torr-1) at 70% BBF if arterial CO2 tension were used to represent the CO2 stimulus but was unchanged if venous CO2 tension were used. At 50% BBF, delta VI/delta PCO2 was depressed (0.38 +/- 0.13 l . min-1 . Torr-1) for both representations of the CO2 stimulus. Brain ischemia increased blood pressure and heart rate but blunted the increase in BBF caused by hypercapnia. We conclude that 1) moderate brain ischemia (70% BBF) does not affect chemosensitivity to hypoxia and CO2, 2) delta VI/delta PCO2 may not be accurately determined from PaCO2 during brain ischemia because cerebrovascular reactivity to CO2 is depressed, and 3) severe brain ischemia (50% BBF) blunts delta VI/delta SaO2 and delta VI/delta PCO2, probably as a consequence of hypoxic depression of the respiratory neurons.
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PMID:Effects of graded reduction of brain blood flow on chemical control of breathing. 53

One hundred consecutive men with a normal ECG at rest had a maximal treadmill test using 14 leads during and post-exercise. Coronary arteriography performed the following day revealed coronary stenoses greater than or equal to 70% in 66 patients. Test results obtained from a V5 lead were compared to different lead combinations and were correlated with arteriographic findings. A positive exercise test occurred in 37 men using an isolated V5 lead compared to 50 men (P less than 0.05) using 11 leads, 52 men (P less than 0.05) using a combined CM5, CC5, Cl (inferior) lead system and 58 (P less than 0.001) men using all 14 leads. The predictive value of a positive test varied between 89-95% and was not changed significantly by the addition of multiple leads. The 14 lead ECG was positive in 43/45 (96%) patients with multivessel disease. Parameters which helped to predict multivessel disease using 14 leads were 1) the time that ischemia first appeared 2) the pressure-rate product at the time ischemia first appeared, and 3) the maximum workload that could be attained. In general, the magnitude of ST-segment depression and the time required for a positive ECG to return to normal postexercise were not useful predictors of multivessel disease. We conclude that the use of multiple leads improves the sensitivity and efficiency of the maximal treadmill exercise test. The usefulness of exercise test results can be further improved if multiple leads are combined with physiologic data collected during exercise.
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PMID:Improved efficiency of treadmill exercise testing using a multiple lead ECG system and basic hemodynamic exercise response. 61


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