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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Junctional ectopic tachycardia after surgical repair of congenital heart defects is associated with high mortality. Usually, it is transitory and resolves spontaneously, but a long period with very fast heart rate and without atrio-ventricular synchrony contraction may cause low cardiac output. Treatment with common anti-arrhythmic drugs is often uneffective both in restoring sinus rhythm and in reducing heart rate. Since hypothermia is known to decrease cardiac automaticity, two infants, aged 4 and 10 months, with junctional ectopic tachycardia and low cardiac output after surgical repair of the atrio-ventricular septal defect were treated with hypothermia after unsuccessful pharmacological attempts to control the arrhythmia. Generalized hypothermia was induced with cooling-blankets and ice packs. Rectal temperature initially dropped to 30 degrees and was subsequently maintained at between 33.8 and 34.2 degrees with the heart rate between 130 and 140 m beats per minute. Trans-oesophageal atrial pacing at a higher rate allowed for sequential atrio-ventricular contraction. Signs of low cardiac output were quickly resolved. One patient was warmed-up after 12 hours of hypothermia and remained in sinus rhythm. In the other patient, the arrhythmia recurred after rewarming and a further 30-hour period of hypothermia was required. Sinus rhythm was maintained thereafter. Both patients are in stable sinus rhythm 20 and 22 months after surgery. Our experience supports the use of hypothermia as a means to control post-operative junctional ectopic tachycardia resistant conventional anti-arrhythmic drugs.
G Ital Cardiol 1990 May
PMID:[Hypothermia treatment of junctional ectopic tachycardia after surgical repair of congenital heart defects]. 221 Jan 63

Isolated rat hearts were used to examine whether reperfusion-induced arrhythmias may be caused by washout of substances accumulating during ischemia. This was achieved by subjecting hearts to 10 min of regional ischemia and rendering them transiently inexcitable during the first 1.5 min of reperfusion. Transient inexcitability was induced by switching to cold solution (4 degrees C) shortly before reperfusion (-1.5 min). In controls (no hypothermia), the incidences of ventricular tachycardia (VT) and ventricular fibrillation (VF) were 83% and 92%, respectively, during the first 1.5 min of reperfusion. Transient hypothermia caused inexcitability and asystole, impaired recovery of coronary flow and abolished VT and VF (all P less than 0.05). On subsequent rewarming to 37 degrees C, coronary flow and sinus rate recovered in all hearts. However, VT and VF occurred in only 58% and 25%, respectively (P less than 0.05). These values were similar to those of new episodes of VT and VF occurring in controls during the equivalent period. Therefore arrhythmias had been abolished during transient hypothermia, not merely delayed. The relative contributions of transient impairment of recovery of coronary flow and transient asystole to the antiarrhythmic effects were examined in a further 10 groups of hearts (n = 12/group) in which reperfusion conditions were transiently manipulated. We utilized combinations of hypothermia, ventricular pacing, acetylcholine (ACh) 55 microM (to cause asystole and impairment of recovery of coronary flow), and right atrial excision and left atrial pacing (to permit bradycardia to be transiently induced during reperfusion by temporarily switching off the pacemaker). The results indicated that transient hypothermia was antiarrhythmic as a result of a reduction of excitability, not because of bradycardia or impairment of recovery of flow. The data support the hypothesis that reperfusion unmasks (disinhibits) latent arrhythmogenic components of ischemia (particularly during the first 1.5 min of reperfusion) and that, by inducing inexcitability, transient hypothermia allows these substances to be washed out without their arrhythmogenic effects being manifested. The identities of the arrhythmogenic and antiarrhythmic substances remain to be determined; we suggest that cyclic AMP and potassium, respectively, are likely candidates.
J Mol Cell Cardiol 1990 Aug
PMID:Are reperfusion-induced arrhythmias caused by disinhibition of an arrhythmogenic component of ischemia? 223 48

By uni- and multivariate analysis, predictors of surgical mortality and postoperative angina were identified retrospectively in 189 patients having had coronary arterial bypass surgery over the period 1978-1984. After modification of these risk factors, surgical outcome was followed up in another 178 patients undergoing operation from 1985 to 1987. The surgical mortality of 7% in the first series was closely associated with postoperative signs of acute myocardial injury. All deaths occurred in patients having at least 3 out of 5 pre- and peroperative risk factors: triple vessel/left main coronary arterial disease, incomplete revascularization, no propranolol treatment, Bretschneider cardioplegia other than "HTP"-solution with blood preperfusion and perioperative vasopressor support. The procedures of cardiac protection were modified. St Thomas multidose potassium cardioplegia and general hypothermia were introduced, perioperative propranolol treatment increased and bypass time decreased. Improved cardiac protection with this regime was seen in the patients operated in 1985-1987 when compared with the first series with regard to perioperative vasopressor support (8 vs 33%, P less than 0.001), spontaneous operative defibrillation (72 vs 52%, P less than 0.001), postoperative arrhythmias (20 vs 43%, P less than 0.001), peak levels of serum enzymes (P less than 0.001), myocardial infarction (7 vs 19%, P less than 0.001) and hospital mortality (2 vs 7%, P less than 0.05). The incidence of freedom from symptoms at 3 months was also increased in the patients undergoing operation from 1985 to 1987 (72 vs 61%, P less than 0.05). Even small centers can improve their surgical outcome by carefully analysing their own results and modifying the identified risk factors.
Int J Cardiol 1990 Jan
PMID:Improved outcome of coronary arterial bypass surgery in a small center after identification and modification of peroperative risk factors. 229 14

Between 1984 and 1988, 15 patients with a type A aortic dissection were treated with direct suturing of the entry opening of the dissection and gluing of the dissected aortic layers using the GRF glue (gelatine-resorcine-formaldehyde), without prosthetic replacement. An associated aortic insufficiency, in 10 patients, was treated with valve replacement (5 patients) or plasty (5 patients). Deep hypothermia with circulatory arrest were necessary in 10 patients whose dissection reached the ascending aorta. All patients survived the procedure. These patients are followed from 6 to 44 months. They are all controlled by echo-Doppler. In addition, ten had an angiography, 6 a control scan and 5 a NMR. In twelve patients, the ascending aorta as well as the aortic junction are normal. A limited aortic dissection which did not require a secondary procedure, is found in 3 patients. A dissection of the descending aorta is present in 10 patients. Two patients had to be re-operated: one, for a valve replacement, 18 months later; the other, for a myocardiopathy at the terminal stage, 14 months later, requiring an orthotopic transplantation. These results show that gluing of the aorta is an easy and effective treatment in type A aortic dissections.
Ann Cardiol Angeiol (Paris) 1990 Jan
PMID:[Treatment of type A aortic dissection by exclusive gluing. Long-term results apropos of 15 patients]. 231 98

A 35-year-old schizophrenic patient was admitted to the Coronary Care Unit with shock, bradycardia and ST-T changes mimicking acute myocardial infarction. The rectal temperature was 33.6 degrees C and the diagnosis of accidental hypothermia was established. Accidental hypothermia must be considered in the differential diagnosis of acute myocardial infarction before instituting thrombolytic therapy.
Int J Cardiol 1990 Aug
PMID:Contraindication to thrombolytic therapy in accidental hypothermia simulating acute myocardial infarction. 239 32

Ca2+-tolerant ventricular myocytes from adult rats were electrically stimulated. The maximal contraction frequency (fm) was determined at different temperatures. In drug-free Tyrode solution, fm follows the Arrhenius equation from 7 to 39.5 degrees C. However, verapamil introduces a discontinuity around 27 degrees C into the Arrhenius plot of fm. Above this transition temperature the calcium antagonist lowers fm more pronouncedly than below. Below, a tenfold higher concentration is needed for the same relative effect as at 37 degrees C. It is argued that this finding might be important in cardiac surgery when calcium antagonists are used for cardioplegia at deep hypothermia.
Basic Res Cardiol 1985
PMID:Temperature dependence of verapamil action. 258 45

The results of open heart surgery in infants have steadily improved. The performance of corrective surgery very early in life has thereby been encouraged. We report four patients who underwent successful surgical correction within 24 h of birth. Two patients with total anomalous pulmonary venous drainage and one patient with pulmonary atresia and intact septum were corrected with the aid of profound hypothermia by the combined surface and bypass cooling technique. Cardiopulmonary bypass alone was used for the fourth patient with aortic stenosis. The usual surgical techniques can be applied successfully to infants even within 24 h of life.
Pediatr Cardiol 1989
PMID:Open heart surgery in the first 24 hours of life. 270 51

To assess the results of operative therapy for permanent junctional reciprocating tachycardia, a type of incessant tachycardia, the clinical and electrophysiologic data of 8 such patients referred for management of tachycardia were reviewed. The duration of incessant tachycardia was 14 +/- 10 years (range 2 to 30). The heart rate at rest during tachycardia ranged from 120 to 150 beats/min. Four of 8 patients had cardiomegaly or depressed ejection fraction (16 +/- 10%, range 5 to 27) at presentation and, of these, 2 had symptoms of congestive heart failure. Exertional dyspnea despite normal left ventricular function was noted in 1 patient, 2 had chronic palpitations and 3 were asymptomatic. Electrophysiologic data confirmed the presence of a posteroseptal pathway with atrioventricular node-like properties conducting slowly in the retrograde direction only. Seven patients underwent successful surgical ablation of the accessory pathway. Hypothermic cardiopulmonary bypass was used in 2 and a closed heart technique without cardiopulmonary bypass in the other 5. Three of 4 patients with reduced left ventricular function showed an improvement in ejection fraction to 34 +/- 20% (range 16 to 63) after control of dysrhythmia. Three patients had no evidence of cardiomegaly despite equivalent periods of incessant tachycardia. Another patient with normal left ventricular function despite incessant tachycardia for over 30 years underwent spontaneous remission to sinus rhythm and did not undergo surgery. These data suggest that permanent junctional reciprocating tachycardia has a variable presentation and that congestive heart failure is not an infrequent presenting symptom. The substrate is invariably an accessory atrioventricular pathway with a long conduction time and decremental properties conducting only in the retrograde direction.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1989 May 01
PMID:Results of operative therapy in the permanent form of junctional reciprocating tachycardia. 270 78

A 66-year-old man having previously undergone repair of aneurysms of the ascending, transverse and infrarenal aorta, presented with a large false aneurysm of the aortic arch. Successful repair of the aneurysm was achieved under a state of profound hypothermia and circulatory arrest. The patient remains well and free from aortic aneurysmal disease two years after surgery.
Can J Cardiol 1989 Apr
PMID:Repair of a false aneurysm of the aortic arch. 272 Apr 79

The surgical treatment of aorto-pulmonary window by a closed technique is described. This avoids the increased risks of extracorporeal circulation and deep hypothermia with or without total circulatory arrest in the neonate or very sick infant.
Pediatr Cardiol 1989
PMID:Surgical closure of aorto-pulmonary window without cardiopulmonary bypass. 199 93


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