bluuebunny/crossref_metadata_2025_split huggingface dataset:
INTRACORONARY STREPTOKINASE INFUSION DURING ACUTE MYOCARDIAL INFARCTION
Authors: Gold Herman K. , Leinbach Robert C. 
Published: August 2010

ABSTRACTRecent angiographic studies have demonstrated that intracoronary thrombus is present in the majority of patients with acute transmural myocardial infarction. In an attempt to overcome coronary artery obstruction and restore antegrade flow, streptokinase has been infused directly into the obstructed coronary artery supplying the infarct zone. We have recently analyzed the angiographic features of 27 patients with acute transmural myocardial infarction presenting within 3 hours of the onset of persistent pain. All underwent coronary angiography and infusion of streptokinase into the occluded coronary artery. Complete occlusion of the left anterior descending coronary artery was seen in all 14 patients with anterior myocardial infarction. Ten of 13 patients with inferior myocardial infarction showed complete right coronary artery occlusion. The remaining 3 patients had subtotal coronary occlusion. At the time of angiography the majority of patients showed an occlusive intraluminal convex filling defect consistent with intracoronary thrombus. Intracoronary nitroglycerin partially restored antegrade flow in only 1 patient with left anterior descending occlusion and in 1 patient with right coronary artery occlusion. Streptokinase was infused at a rate of 2,000–6,000 IU/ minute. In 20 of 27 patients (74 %) antegrade coronary flow was reestablished within 1 hour of streptokinase infusion. Chest pain was relieved and ST segments were reduced in most, but not all, of these patients. After intracoronary streptokinase infusion, the residual coronary artery stenosis was greater than 60 % in all patients. Two patients demonstrated acute reocclusion at the completion of streptokinase infusion. Five of 20 patients (25 %) developed late reocclusion 4 days to 3 months after successful clot lysis. Coronary patterns associated with reocclusion include ulcerated plaques, multiple distal vessel stenoses, irregular residual stenosis of greater than 90 %.In conclusion, angiographic studies support the hypothesis that an occlusive intracoronary thrombus is the cause of persistent myocardial injury in many patients with acute myocardial infarction. In the majority of cases, intraluminal thrombus can be identified as a convex filling defect. Selective coronary angiography can be performed safely during the acute phase of myocardial infarction and provides important information regarding the nature of the obstructive lesion in the vessel supplying the infarct zone. The benefits of early angiography and administration of intracoronary thrombolytic therapy requires further study.
NITROGLYCERIN IN THE TREATMENT OF ACUTE MYOCARDIAL INFARCTION
Authors: Bussmann Wulf‐Dirk 
Published: August 2010

SUMMARYNitroglycerin and nitrates have long been contraindi‐cated in the treatment of acute myocardial infarction because of the possibility of an undesirable decrease in arterial blood pressure and the induction of cardiogenic shock. Nowadays nitroglycerin seems to be indicated at least in subgroups of patients with acute myocardial infarction. Intravenous nitroglycerin reduce left ventricular filling pressure up to 40% within several minutes. The effect is most pronounced if filling pressure is elevated. There is no decrease in arterial pressure with low dosage nitroglycerin and a 10 % decrease with higher dosages. Cardiac output and stroke volume were found to increase following nitroglycerin application in patients with left ventricular failure. This may be due to the improved regional ventricular function in areas with decreased coronary flow. A slight, but significant decrease in cardiac output was found in patients not in failure. Nitroglycerin seems to be the drug of choice in acute pulmonary edema, because of its internal bloodletting effect. Following sublingual nitroglycerin, left ventricular filling pressure decreased within 3–5 minutes in conjunction with clinical improvement of the patient.High blood pressure in such patients is largely reduced. — Nitroglycerin, therefore, seems to be applicable even in patients with acute and marked arterial hypertension.Clinical improvement was evident in patients with dyspnea or pain following myocardial infarction. The need for morphine was reduced. Myocardial ischemia as assessed by electrocardiographic ST‐segment elevation improved following application of nitroglycerin. This effect is more pronounced in patients with left ventricular failure.In a randomized prospective study, 31 patients received intravenous nitroglycerin at least for 2 days and were compared to 29 patients with no specific therapy. CK and CKMB infarct size was 30 % less than in the control group. Even with nitroglycerin administration 8 hours after the onset of symptoms, CK and CKMB activities were significantly reduced.Preliminary results showed early mortality to be reduced in patients receiving nitroglycerin; The rate of reinfarction also was lower. The incidence of angina pectoris 1 1/2 years after the infarct, however, was higher in patients receiving nitroglycerin therapy initially. Following infarct size reduction more ischemic myocardium remains, possible indication for further therapy such as bypass surgery. The improvement in myocardial ischemia seems to be the reason for the reduction in ventricular ectopic beats during treatment. The need for lidocaine was markedly reduced. Even bradycardia seems to be improved, since the use for atropine was only half that for the control patients. These results provide evidence that nitroglycerin and nitrates appear to be indicated in patients with acute myocardial infarction, especially in those with left ventricular failure.
Myocardial Catecholamines and Their Biosynthetic Enzymes in Various Human Heart Diseases
Authors: Siltanen P. , Penttilä O. , Merikallio E. , Kyösola K. , Klinge E. , Pispa J. 
Published: August 2010

ABSTRACT.Myocardial noradrenaline (NA) content, together with the activities of the enzymes tyrosine hydroxylase (TH) and dopamine beta–hydroxylase (DBH) was measured in biopsy specimens taken during cardiac surgery from patients with various heart diseases. Fluorescence histochemical studies were also performed on comparable specimens.The mean NA content in patients with symptomatic ischaemic heart disease (IHD) was significantly higher than that in patients with valvular heart disease (VHD), atrial septal defect (ASD) or congestive heart failure (CHF). The lowest mean NA content was found in patients with CHF. The activities of TH and DBH were highest in the IHD group, although the differences between IHD and VHD groups were not significant. Histochemical investigations of adrenergic structures showed less fluorescence intensity in the CHF than in the other 3 groups. On the other hand, the density of the adrenergic nerve net and the size and number of varicosities were greatest in patients suffering from IHD.The significance of these results is discussed in relation to the pathophysiological mechanisms underlying these various disease conditions. In IHD the high myocardial NA content creates local conditions for excessive NA release into the myocardial interstitium at the onset of ischaemia, which is known to result in several adverse local consequences.
Psychological Risk Factors Related to Coronary Heart Disease. Prospective Studies Among Policemen in Helsinki
Authors: Nirkko O. , Lauroma M. , Siltanen P. , Tuominen H. , Vanhala K. 
Published: August 2010

ABSTRACT. Psychological investigations carried out on 1326 Helsinki policemen showed that individuals with electrocardiogram (ECG) signs of coronary heart disease (CHD), and those showing symptoms, were more anxious, aggressive, defensive and inhibited than those free from signs or symptoms. It is suggested that the poor prognosis associated with angina pectoris may be related to the psychological characteristics of the patients who suffer from it.Studies of 5– and 10–year prospective data showed that subjects dying from myocardial infarction differed from survivors on six significant psychological characteristics, including optimism, inhibition and superego strength. Multiple logistic analysis showed an association of lowered self–esteem and high somatization with myocardial infarction.A particular statistical analysis (»ridit analysis«) revealed the existence of 4 variables (inhibition, neuroticism, differentiaton and certainty) which distinguished to some degree with different manifestations of CHD. The nature of these variables and the correlations involved are discussed. It is concluded that psychological variables have some predictive power not only for the risk of CHD, but also for the risk of clinically different CHD events.
The Recurrent Coronary Prevention Project. Some Preliminary Findings
Authors: Thoresen Carl E. , Friedman Meyer , Gill James K. , Ulmer Diane K. 
Published: August 2010

ABSTRACT. The Recurrent Coronary Prevention Project (RCPP) was established as a 5–year clinical trial to examine two basic questions: –

Can the recurrence rate of post–coronary subjects be substantially reduced over a 5–year period by means of a programme of behavioural change, in comparison with treatment by cardiologists focussing on medication, diet, exercise and cardiovascular issues, and with subjects who only receive regular care from their own physician?
Can the Type A behaviour pattern (TABP) be changed and do such changes correspond to reduced recurrences of coronary heart disease (CHD) over a 5 year period?

To answer these questions, four major treatment groups are currently being compared: –

A small group treatment programme (Section I) led by cardiologists emphasizing adherence to medication, diet and exercise, and giving cardiovascular and cardiological information.
A behavioural change treatment programme (Section II) based primarily on a cognitive social learning model and attempting to alter TABP.
A control group of subjects assessed annually and receiving private medical care from their own physicians.
A dropout comparison group composed of subjects voluntarily discontinuing participation in groups led by cardiologists or in behavioural change groups.

Results to date show a significantly reduced rate of recurrence for subjects in the behavioural change group, compared to those in the groups led by cardiologists as well as control and dropout groups. These significantly lower recurrence rates are accompanied by data suggesting that subjects in the behavioural change programme are also altering their TABP as measured by both behavioural questionnaires and videotaped Type A structured interviews. Clinical impressions suggest that treatment programmes to alter TABP should consider the primary importance of the personal meaning of the TABP and other behaviours to the individual concerned, particularly how basic underlying beliefs set the stage for the TABP. The central role of hostility as a pervasive orientation towards self and others is emphasized, as are issues of excessive controllability related to extreme competitiveness and hyper–arousal. The multiple roles of group leaders, especially as social models for coping, and the impact of the small groups settings, is also discussed.The data generally demonstrate the emerging advantage of a behavioural change treatment programme with respect to the observed reduction in recurrence rates and provide preliminary evidence of reduced levels of the TABP in subjects receiving such treatment. Whether these findings will be substantiated and maintained over the full 5–year period and thereafter remains to be established.
Metabolic effects of β–adrenoceptor blockade on skeletal muscle at rest and during exercise
Authors: Juhlin–Dannfelt Anders 
Published: August 2010

ABSTRACT. β–adrenoceptor antagonists influence the metabolic responses in man at rest and during exercise. Impaired working capacity and muscular fatigue have been reported in patients on β–blockers and this could be due to an altered substrate supply to the muscles.The results from several studies show that the main effect of β–blockade on metabolism is decreased lipolysis, with less fat available to the muscles. This results in an increased carbohydrate demand to maintain an unchanged aerobic metabolism, and liver and muscle glycogen stores are more rapidly depleted, β–blockade also results in decreased lactate release from the muscles, probably due to a membrane effect and/or changed perfusion.It is concluded that β–blockade a) decreases fat metabolism in the muscle, which secondarily increases the use of carbohydrates during exercise, resulting in earlier hypoglycaemia and/or depletion of muscle glycogen with reduction of the working capacity, b) impairs lactate transport from the muscle but does not cause lactate accumulation within the muscle which could be responsible for muscular fatigue.
Labetalol in the treatment of hypertension in patients with normal and impaired renal function
Authors: Walstad Rolf A. , Berg Knut J. , Wessel–Aas Terje , Nilsen Odd G. 
Published: August 2010

ABSTRACT. Labetalol (Trandate) is a new antihypertensive agent with both α– and β–adrenoceptor blocking properties. In a dobule–blind cross–over study the antihypertensive action and side–effects of labetalol and propranolol were compared in 18 previously untreated outpatients with hypertension, WHO stage I–III. Mean daily dose of labetalol was 667 mg and of propranolol 129 mg. Labetalol reduced systolic and diastolic blood pressure in the seated and upright position significantly more than propranolol. The pulse rate reduction was greater with propranolol. Side–effects were more pronounced with propranolol.The antihypertensive effect, effect on pulse rate and pharmacokinetics of a single oral dose of 400 mg labetalol were studied in 6 patients with normal and 6 patients with impaired renal function (creatinine clearance < 20 ml/min), all belonging to WHO stage I–II. A significant fall in pulse rate and systolic and diastolic blood pressure was observed in both groups, the duration being more than 25 h. No difference was found between the two groups. From the serum concentration–time curves the elimination rate constant, elimination half–life and area under the curve were calculated. The mean values of the two groups did not differ significantly. A pronounced interindividual variation was found in both groups.
The haemodynamic effects of intravenous prenalterol and ouabain in conscious dogs
Authors: Ek L. , BJörkman J.–A. , Carlsson E. , Johansson B. 
Published: August 2010

ABSTRACTExperiments were performedon5 resting conscious dogs supplied with an electromagnetic flow probe on the ascending aorta and a chronic aortic catheter for pressure recording. The animals were used repeatedly in four different types of experiment involving i. v. administration of1.saline (controls),2.prenalterol 45 nmol/kg (∞ 10 μg/kg) followed by an additional dose of 135 nmol/kg 20 min later,3.ouabain 50 nmol/kg (∞30 μg/kg) and4.a combination of protocols2.and3.Ouabain and the low dose of prenalterol exerted clear–cut positive inotropic effects as reflected in increased stroke volume and max dF/dt without significant changes in heart rate or arterial pressure. The PQ interval increased with ouabain but decreased with prenalterol. The higher dose of prenalterol caused a further rise in max dF/dt, a further shortening of the PQ time, increased heart rate and reduction in systemic vascular resistance. Higher doses of ouabain could not be given due to side–effects (vomiting). The combined treatment with ouabain and prenalterol showed their inotropic responses to be additive. Arrhythmias did not occur in any of the animals at the applied dose levels of the drugs. The experiments show that prenalterol through its β1–adrenoceptor stimulating action exerts a positive inotropic effect which surpasses that of emetic doses of ouabain. The inotropic response at moderate doses occurs without a change in heart rate. This fact and the apparent lack of influence of prenalterol on vascular α– and β2–adrenoceptors make the substance potentially useful clinically as an inotropic agent in cardiac failure, particularly in view of its relatively long duration of action.
Prenalterol as an antidote to massive doses of meto–prolol – a cardiovascular study in the dog
Authors: Andersson T. , Heath A. , Mattsson H. 
Published: August 2010

ABSTRACTFourteen beagle dogs were treated with increasing doses of metoprolol. The first group (n=7) formed part of a preliminary study to establish a suitable dosage regimen. Two of these dogs recovered from plasma concentrations of about 50 000 nmol/1 metoprolol, when metoprolol infusion was stopped. Pour dogs died with plasma concentrations of about 80 000 nmol/1 metoprolol and one dog, in which AV block II developed, recovered from a CO of 300 ml/min after 10 mg/kg prenalterol.The second group consisted of a control group of three dogs and a prenalterol treated group of four dogs. Both groups were treated with increasing doses of metoprolol for 1.5 hours followed by a continuous infusion of metoprolol throughout the rest of the experiment, reaching plasma concentrations of 50 000 nmol/1 of metoprolol. In the prenalterol group, prenalterol was given i.v. in a dose of 0.5 mg/kg every 10 minutes starting 3 hours after the first dose of metoprolol up to a total dose of 5 mg/kg.Metoprolol caused an initial decrease in heart rate (HR) which remained stable at 115 beats/min despite increasing plasma concentrations. Blood pressure (BP) and cardiac output (CO) fell, the decrease being directly proportional to plasma concentrations of metoprolol. The central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) increased indicating reduced inotropic function of the heart. An initial increase in total peripheral resistance (TPR) was seen followed by a return to almost baseline levels with increasing metoprolol concentrations. The three control dogs died after 4–5 hours. Death was caused by low CO failure, preceded by nodal bradycardia followed by asystole. No characteristic ECG changes were seen until cardiac failure developed. Prenalterol reversed the effect of metoprolol on CO, stroke volume (SV), CVP and PCWP. BP and HR remained below the basal values. These basal values of BP and HR were, however, high because of increased sympathetic activity caused by the chloralose anaesthesia. The return of TPR to basal values was more pronounced in the prenalterol group than in the control group.The results suggest that neither HR nor ECG can be used to assess the severity of metoprolol poisoning. BP and CVP or PCWP and when possible CO are probably the best clinical aids in assessment.The present study shows that prenalterol by exerting a pronounced inotropic effect can completely reverse the low CO failure caused by massive doses of metoprolol. However, doses of prenalterol much higher than those normally used are necessary.
The hemodynamic actions of prenalterol in left ventricular failure
Authors: Awan N. A. , Evenson M. K. , Needham K. E. , Mason D. T. 
Published: August 2010

ABSTRACTThe hemodynamic effects of prenalterol, a parenteral cardioselective β1–receptor agonist, were evaluated by cardiac catheterization in patients with refractory severe congestive heart failure (CHP). Prenalterol (PN) (4 mg i.v.) did not alter (p > 0.05) heart rate (HR), mean blood pressure (MBP) or left ventricular filling pressure (LVPP). Concomitantly PN markedly augmented cardiac index (CI) from 1.9 to 2.6 1/min/m2 (p < 0.01) and substantially elevated stroke index (SI) from 24 to 30 ml/beat/m2 p < 0.001). In addition PN raised stroke work index (SWI) from 21 to 26 g.m/m (p < 0.005) and decreased total systemic vascular resistance (TSVR) from 1702 to 1260 dyn.s.cm−5 (p < 0.001). An important finding was that the heart rate × systolic blood pressure product was unchanged (p > 0.05) and precipitation of cardiac dysrhythmias or myocardial ischemia were not observed.Further PN 1 mg, 4 mg and 8 mg i.v. was sequentially injected and peak hemodynamic effects were determined 10 min after drug administration. PN 1 mg raised CI from 2.1 to 2.5 1/min/m2 (p < 0.01), elevated SI from 24 to 29 ml/beat/m2 (p < 0.01), and augmented SWI from 21 to 25 g.m/m2 (p < 0.01), however, TSVR declined from 1702 to 1392 dyn.s.cm−5. Subsequent incremental PN doses of 4 and 8 mg did not provide (p > 0.05) additional enhancement of cardiac function.Thus, prenalterol produced markedly beneficial enhancement of cardiocirculatory function without untoward effects and may be useful in the management of patients with severe congestive heart failure. Moreover, dose–response analysis indicates these salutary improvements can be maximally produced by the small dose of 1 mg obviating the need for larger doses.
Intravenous prenalterol in acute and chronic heart failure
Authors: Kirlin P. C. , Pitt B. , Lucchesi B. R. 
Published: August 2010

ABSTRACTThe new inotropic agent prenalterol was administered intravenously in a canine model of acute ischemic heart failure and in patients with severe chronic heart failure. Experimental heart failure in anesthetized dogs was induced by two vessel coronary artery constriction and intravenous prenalterol (0.005–15 μg/kg/min) was compared to dobutamine (0.001–30 μg/kg/min) and saline. Significant dose–dependent increases in left ventricular dP/dtmax′ cardiac output and non–ischemic zone contractile force and significant reductions in systemic vascular resistance were present during infusions of both inotropic agents. High dose dobutamlne caused greater increases in mean arterial pressure and pressure rate product with a trend toward greater increases in heart rate. However, neither inotropic agent significantly improved ischemic zone contractile force. Prenalterol possessed a markedly longer hemodynamic half–life than dobutamlne (3.0 hours compared to 1.7 minutes).Nine patients with severe chronic heart failure (left ventricular ejection fraction mean ± SD 17 ± 5%, cardiac index 1.7±0.4 1/min/m2) responded to intravenous prenalterol (1, 4, and 8 mg) with significant increases in cardiac index, left ventricular ejection fraction and left ventricular stroke work index. Left ventricular filling pressure, mean right atrial pressure and pulmonary arteriolar resistance were significantly reduced. No significant differences were present among peak responses to the three doses employed. An inverse correlation between basal heart rate and increase in left ventricular ejection fraction following prenalterol was noted.The mechanisms by which prenalterol causes hemodynamic improvement appear to include a direct inotropic effect, a reduction in left ventricular outflow resistance and a reduction in left and right ventricular filling pressure (venodilating effect). The net result is an upward and leftward shift of the depressed ventricular function curve.Both prenalterol and dobutamine were associated with sustained ventricular tachyarrhythmias in the experimental acute low output state and two digitalized patients with ischemic cardiomyopathy developed transient ventricular tachycardia after prenalterol administration. These findings indicated that adrenergic stimulants should be administered in severe ischemic states with careful monitoring.