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Biomedical subjects

Y Hasin

Publications and source records attributed to Y Hasin.

At least 91 records · Page 5Linked to original sources
PubMed1987

Prehospital coronary thrombolysis. A new strategy in acute myocardial infarction.

Thirty-four patients with acute myocardial infarction were treated prospectively using a new strategy of prehospital intravenous streptokinase given by a physician-operated mobile intensive care unit. The 29 prehospital-treated patients who had experienced no previous myocardial infarction were compared to a similar group treated with streptokinase inhospital. Patients receiving streptokinase in the prehospital phase of acute myocardial infarction had smaller infarcts and better residual myocardial function than the group given streptokinase inhospital in terms of peak creatinine phosphokinase, ejection fraction, computer-derived dysfunction index, and electrocardiographic QRS score. The only difference between these groups at baseline was the duration of pain prior to initiation of streptokinase therapy. There were no major complications related to prehospital administration of streptokinase.

Aged↗
PubMed1987

Fat-free diet and myocardial excitability, refractoriness and ventricular fibrillation.

The lipid composition of the sarcolemma influences its function. The purpose of this study is to investigate the electrophysiological alterations induced in the rat's heart by dietary manipulation of cardiac fatty-acid composition. Strength-duration and strength-interval relationships were used to study excitability and refractoriness respectively. Ventricular fibrillation threshold measured by short bursts of rapid stimulation was used to indicate ventricular vulnerability. Gas liquid chromatography was used to analyse cardiac fatty-acid-composition. We used two-week-old rats fed with fat-free diet and 5% and 10% soya bean oil-supplemented diets for 6-9 weeks. Fat-free diet only was associated with increased eicosatrienoic acid content, a marker of essential fatty-acid deficiency. A decrease in poly-unsaturated to saturated (P:S) fatty-acid ratio was also observed. Five percent oil supplementation was associated with a delay and attenuation of this effect. Fat-free diet was associated with increased excitability, decreased refractoriness and reduced ventricular fibrillation threshold. Ten percent oil supplementation prevented these effects while 5% oil supplementation had only a temporary protective effect. We conclude that manipulation of dietary fat content can affect cardiac fatty-acid composition and electrophysiology.

Animals↗
PubMed1987

Influence of vessel involvement and early streptokinase therapy on regional and global left ventricular function in acute myocardial infarction.

150 consecutive patients with acute myocardial infarction received 750,000 units of intravenous streptokinase within four hours of pain onset. Angiography was performed on day 6, from which ejection fraction (EF), infarct-related ejection fraction (IREF), and non-infarct related ejection fraction (NREF) were calculated. 50% stenosis was considered to be significant. The streptokinase patients with patent infarct-related arteries who had no evidence of previous myocardial infarction were compared with 82 conventionally treated (without streptokinase) patients who had no evidence of previous myocardial infarction. Sub-group analysis based on vessel involvement, usage and timing of streptokinase was done. Streptokinase was associated with better left ventricular function in all sub-groups if given less than 2 hours after pain onset. In inferior myocardial infarction, streptokinase patients with single-vessel disease had normal EF (67 +/- 8), compared to significantly depressed EF in multi-vessel disease (56 +/- 12, p less than 0.05). This difference is accounted for more by the NREF than the IREF. In anterior infarction, patients with single-vessel disease did only slightly better than multi-vessel disease. In multi- and single-vessel anterior infarction, preservation of function by streptokinase appears to be due to the compensatory ability of the non-infarcted region as well as the residual function of the infarct-related region. region.

Cardiac Output↗
PubMed1987

Dietary lipid intake and myocardial electrophysiology.

We studied the effect of a fat-free diet on the cardiac electrophysiology of rats. Fourteen 2-week-old rats were maintained on a fat-free diet and 12 rats had a 5% soybean oil supplement to their diet. The rats were killed after 6 weeks and the hearts mounted on a Langendorff chamber. Atrioventricular (A-V) block was induced. Myocardial strength-duration (S-D) and strength-interval (S-I) curves were determined. A significant depletion of linoleic acid and elevation of palmitoleic, stearic, and oleic acids was found in the hearts obtained from rats on fat-free diet as compared with the hearts obtained from the rats on oil-supplemented diets. Hearts obtained from rats who had had the oil supplement had a shorter refractory period and an increased threshold for excitation; therefore, these hearts should be less vulnerable to cardiac dysrhythmias. Both S-D and S-I curves best fitted a logarithmic relationship. The intercepts and slopes of these curves were significantly different in the two groups. There were significant correlations between myocardial fatty acid composition (stearate and linoleate in particular) and the different electrophysiological parameters.

Animals↗
PubMed1986

Importance of early initiation of intravenous streptokinase therapy for acute myocardial infarction.

The importance of timing of intravenous streptokinase (SK) administration in patients with acute myocardial infarction (AMI) was evaluated. Intravenous SK, 750,000 U, was administered within 4 hours of the onset of ischemic chest pain to 72 consecutive patients having their first AMI. Six days later, cardiac catheterization was performed to calculate global ejection fraction (EF), and computer-derived infarct-related regional EF and dysfunction index were also determined; electrocardiograms were recorded, from which QRS scores could be calculated to estimate infarct size. Of 19 patients who had an anterior AMI, 12 (63%) who received intravenous SK within 2 hours after onset of pain sustained only minimal damage in terms of global EF, infarct-related EF, dysfunction index and QRS score. All 10 patients who received SK 2 to 4 hours after pain onset had large infarcts (p less than 0.001). Of the former group, 11 of 12 patients (91%) whose pain was relieved within 1.5 hours of intravenous SK administration (presumably due to successful reperfusion) had a good outcome, whereas all 7 whose pain lasted longer did poorly (p less than 0.001). Furthermore, among patients with anterior AMI, 11 of 14 (79%) whose pain was relieved within 3.5 hours of onset had small infarcts, compared with none of the 12 patients whose pain lasted longer (p less than 0.0001). In inferior AMI, the critical time between onset of pain and initiation of intravenous SK was 1.5 hours (p less than 0.05). The timing of initiation of thrombolytic therapy and the total pain duration are critical in determining outcome in AMI, and time intervals vary depending on infarct localization.

Aged↗
PubMed1986

Bradycardia and hypotension following reperfusion with streptokinase (Bezold-Jarisch reflex): a sign of coronary thrombolysis and myocardial salvage.

Acute myocardial infarction, particularly of the inferior wall, is frequently associated with bradycardia and hypotension. This study reports the occurrence of transient bradycardia hypotension (TBH) (Bezold-Jarisch reflex) following thrombolytic therapy with intravenous streptokinase. Of the 52 patients, 42 had successful reperfusion, and 12 of the latter developed reflex TBH. The Bezold-Jarisch reflex occurred in 10 of 24 patients with inferior wall acute myocardial infarction and in 2 of 28 patients with anterior wall infarction (p less than 0.05). The reflex was associated with significantly more non-Q wave infarctions (p less than 0.05) and also with reduction of left ventricular damage, as evidenced by a lower QRS score (4 +/- 3.8 vs 8.9 +/- 5.6, p less than 0.01) and a higher ejection fraction (61 +/- 13% vs 49 +/- 16%, p less than 0.05). Patients with inferior wall acute myocardial infarction were divided into those with TBH (10 patients) and those without TBH (14 patients). TBH was associated with a significantly higher infarct-related regional ejection fraction (60 +/- 19% vs 35 +/- 18%, p less than 0.05). The results of this study confirm previous findings that reperfusion of the inferoposterior myocardium is capable of stimulating reflex TBH. Furthermore, TBH is associated with patency of infarct-related coronary arteries and myocardial salvage.

Adult↗
PubMed1986

T-2 toxin effect on cultured myocardial cells.

Beat rate, contractility and viability of cultured myocardial cells perfused with solutions containing various concentrations of T-2 toxin were studied. While doses below 50 micrograms/ml had no immediate effect, those above 250 micrograms/ml decreased beat rate and amplitude. After 10-30 min of perfusion most cells stopped beating and did not restart after withdrawal of toxin. Nevertheless, most cells remained viable as judged by morphology and trypan blue exclusion. A 24-h exposure to doses of 5 or 2.5 micrograms/ml of toxin decreased the beat rate and inotropic responses of the myocytes. After 48 h cell death ensued. Thus T-2 toxin has some direct toxicity to myocardial cells but the lethal dose seems too high to make this the cause of cardiovascular failure.

Animals↗
PubMed1986

Feasibility of pre-hospital fibrinolytic therapy in acute myocardial infarction.

Intravenous streptokinase (STK) was given in the field by a physician-staffed mobile intensive care ambulance to 13 patients. Patients waited 33 +/- 17 minutes to call the ambulance, arrival time was 5 +/- 3 minutes, and a further work-up time of 32 +/- 8 minutes elapsed. The average time from the onset of pain until administration of STK was 66.7 minutes. Patients were transferred to hospital without important side effects or complications. Eleven of 12 of the infarction-related arteries were patent on subsequent coronary angiography. Three patients had minor hematomas and two had microscopic hematuria. This pilot study shows that intravenous STK can be given with relative ease and safety at home by an experienced physician capable of treating any complications.

Adult↗
PubMed1986

Heat acclimation: cardiac performance of isolated rat heart.

Cardiac performance was studied in the isolated perfused hearts of rats heat acclimated at 34 degrees C (AC) and their age-matched controls (C). The pressure-volume curves during isovolumetric conditions showed a shift to the right in AC compared with C hearts. At similar left ventricular (LV) volumes end-diastolic and peak systolic pressures of AC hearts were lower, but no difference was observed in the maximal pressure developed at the highest LV volumes measured. In both C and AC hearts the developed force decreased as pacing rate increased. AC and C heart responses were the same up to 250 pulses/min. At higher frequencies the amplitude of the developed force of AC hearts was smaller than that of the controls. In accordance the tension produced by very early premature beat reduced in AC compared with C hearts. Since no hypertrophy was observed in AC hearts, it is concluded that heat acclimation results in a change in the intrinsic properties of the AC hearts exhibited by increased compliance, reduced chamber stiffness, and a decrease in the tension developed for each volume load. It is also suggested that at a high beating rate AC hearts fail to restitute its contractility as quickly as C hearts.

Acclimatization↗
PubMed1986

Histologic evidence for small-vessel coronary artery disease in patients with angina pectoris and patent large coronary arteries.

We studied six patients who suffered from angina pectoris but had angiographically patent major coronary arteries. Two of the patients suffered also from congestive heart failure. Three patients had supraventricular tachyarrhythmias. Three patients had conduction disturbances. During coronary angiography the patients had significantly reduced flow velocity of angiographic contrast medium compared with that in a control group. Echocardiographic and Doppler flow studies showed a tendency for symmetrical thickening of the left ventricular wall, enlargement of the right ventricle, and reduced compliance of both ventricles. Right ventricular endomyocardial biopsy revealed pathologic small coronary arteries with fibromuscular hyperplasia, hypertrophy of the media, myointimal proliferation, and endothelial degeneration. Capillaries had swollen endothelial cells encroaching on the lumen. Myocardial hypertrophy, lipofuscin deposition, and patchy fibrosis were also observed. These cases show that small-vessel coronary artery disease can cause classic angina pectoris. The diagnosis can be suspected when the coronary angiogram shows large patent arteries with slow flow of the angiographic contrast medium and it can be confirmed by endomyocardial biopsy.

Adult↗
PubMed1986

Left ventricular function in acute myocardial infarction: assessment by nuclear angiography.

Left ventricular function was assessed in 38 patients two to six days after acute myocardial infarction using nuclear angiocardiography and the following parameters were measured: Left ventricular end-diastolic (LVEDV) and end-systolic volumes (LVESV), ejection fraction (LVEF), indices of left ventricular filling and emptying, right ventricular ejection fraction and ejection rate. Their clinical significance was assessed by their relationship to the patients site and size of infarction, functional capacity, morbidity and mortality. The most sensitive indices of depressed left ventricular function were the EF and ESV. Thus, function was preserved in patients with a small inferior infarction (LVEF = 0.57 +/- 0.07, LVESV = 69 +/- 14 ml) and in Killip Class I (LVEF = 0.48 +/- 0.13, LVESV = 80 +/- 20 ml). Function was disturbed most in patients with extensive anterior infarction (LVEF = 0.18 +/- 0.12, LVESV = 131 +/- 46 ml), Killip Class IV (LVEF = 0.13 +/- 0.07, LVESV = 160 +/- 35 ml), cardiogenic shock (LVEF = 0.14 +/- 0.07, LVESV = 160 +/- 35 ml), pulmonary edema (LVEF = 0.11 +/- 0.06, LVESV = 166 +/- 25 ml) and pulmonary capillary wedge pressure greater than 20 mm Hg (LVEF = 0.14 +/- 0.07, LVESV = 160 +/- 33 ml). Previous infarction was associated with LV dilatation and a greater LVEDV. A lower ejection fraction signified a large infarct and poor left ventricular function. If the ejection fraction was less than 0.15, the patients were unlikely to leave the hospital alive, or if less than 0.25, they were left with poor residual ventricular function and either had significant cardiac failure or high late mortality. Nuclear angiocardiography was a simple method of predicting the clinical pattern and prognosis in each patient and emphasized the importance of limiting infarct size in acute myocardial infarction.

Adult↗
PubMed1986

Atrial fibrillation in acute myocardial infarction.

Atrial fibrillation (AF) complicating acute myocardial infarction (AMI) is associated with increased morbidity and mortality. Early intervention with antiarrhythmic treatment and hemodynamic support in patients prone to develop AF may modify their course. The purpose of this study was to characterize on admission the patients with AMI who are prone to develop AF. The admission data of 45 consecutive patients who developed AF during the course of AMI, and the data of a control group of 45 consecutive patients with AMI who did not develop AF, were analyzed using logistic regression. The following characteristics of patients who developed AF were identified: old age, history of heart failure prior to admission, low systolic blood pressure on admission, wide P waves, presence of left bundle branch block or left anterior hemiblock, marked ST segment elevation, and PQ segment depression (admission ECG). The logistic regression formula correctly classified 80 of the 90 patients (89%) to their actual group. The study showed that the relative risk of a patient with AMI to develop AF can be estimated on admission from simple, readily available, clinical data.

Aged↗
PubMed1986

Deferoxamine improves left ventricular function in beta-thalassemia.

Serial echocardiographic examinations were made to study the changes in left ventricular (LV) function and wall mass in 35 patients with thalassemia followed up for 5.5 +/- 2 years (mean +/- SD). Twenty patients received deferoxamine sulfate for 2.0 +/- 0.6 years (drug group) and 15 patients did not (nondrug group). Repeated blood transfusions were used to maintain the pretransfusion hemoglobin levels at 9 g/dL (90 g/L). Deferoxamine therapy improved LV function and decreased LV wall mass. Percentage shortening of LV diameter improved in the drug group (5.0% +/- 3.9%) and deteriorated in the nondrug group (-6.8% +/- 5.6%). Similarly, the maximum velocity of LV posterior wall motion improved in the drug group (16.1 +/- 20.1 mm/s) and deteriorated in the nondrug group (-18.3 +/- 19.0 mm/s). Left ventricular wall mass decreased in the drug group when compared with the nondrug group. In a subset of the drug group, pathologic natural deterioration in LV systolic function was reversed by treatment. Correlation studies indicated that frequent blood transfusions together with chelation therapy reduced LV dilatation and wall thickness, but blood transfusions alone did not have the same effect. Thus, treatment of patients with thalassemia with modest blood transfusions and deferoxamine can prevent deterioration and may even improve their LV systolic function, associated probably with arrest and reversal of the pathologic process that increases LV wall mass.

Adolescent↗