Myocardial infarction--coronary care.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S Holmberg.
Explore the source record for details and available documents.
Although vasodilators may be of value in treating hypertension and heart failure, excessive vasodilation may worsen poststenotic myocardial perfusion in patients with coronary artery disease. In this study, 11 patients with ischemic heart disease were given 0.010, 0.015, and 0.025 mg/min of felodipine, a potent arteriolar dilator, and hemodynamics and myocardial lactate extraction were measured. Plasma concentrations at the three dose levels (D1, D2, and D3) were 11 +/- 4, 22 +/- 5, and 40 +/- 8 nmol/l, respectively. Mean heart rate rose from 61 +/- 13 to 79 +/- 10 beats/min at D3 (p less than 0.01) and mean arterial pressure was reduced from 113 +/- 25 to 86 +/- 13 mmHg (p less than 0.01). There was a marked increase in cardiac index at all three dose levels (p less than 0.05 to p less than 0.01). The systemic vascular resistance was reduced by 47% at D3 and coronary vascular resistance by 44% (both p less than 0.01). Myocardial oxygen consumption was not changed by felodipine. There were three patients with myocardial lactate production both before and after drug administration, but there were no ST-segment shifts or chest pain in any patient. In conclusion, felodipine seems to be a potent vasodilator and deterioration of myocardial metabolic function occurs infrequently. Our results suggest that felodipine can be safely administered even in high doses to patients with severe coronary artery diseases.
The haemodynamic effects of felodipine 0.1 mg/kg p.o., a new arteriolar dilator, were studied in 7 patients with severe congestive heart failure of NYHA Class IV (Group A) and in 3 patients in Class II-III (Group B). In Group A, measurements were made before and 1 and 4 h after felodipine administration. There was a substantial fall in systemic arterial pressure, which was not associated with a compensatory tachycardia. In fact, there was a fall in heart rate from 92 to 82 beats/min 1 h after drug administration. The pulmonary capillary wedge pressure was reduced from 22 to 14 mm Hg and the cardiac index and stroke volume index rose significantly. Consequently, there was a marked reduction in systemic vascular resistance. In Group B measurements were performed at rest and during exercise before and 1 h after felodipine. The pulmonary wedge capillary pressure during exercise was lower than in the control situation. Coronary sinus flow was increased and there was a pronounced fall in coronary vascular resistance. The results would suggest that felodipine, by virtue of its ventricular unloading potency, might be a valuable drug in the treatment of congestive heart failure.
A 39-year-old woman had suffered from congestive heart failure of unknown cause for 3.5 years before a phaeochromocytoma was diagnosed. After pretreatment with phenoxybenzamine, the tumour was removed by surgery resulting in disappearance of signs of heart disease. The patient was followed for 16 years: at that time she was free of symptoms and X-ray and echocardiography showed only a slightly enlarged heart and a minor impairment of left ventricular performance. Six similar cases from the literature are reviewed. The significance of catecholamines in causing heart disease in patients with phaeochromocytoma is discussed.
A double-blind trial with the beta 1-selective blocker metoprolol in suspected acute myocardial infarction and during 3 months' follow-up included 1395 patients, aged 40-74 years, 698 on metoprolol and 697 on placebo. In order to further evaluate the tolerability to beta-blockade in the elderly, the total series was divided into 2 groups according to median age (61 years) and into quartiles, the lowest quartile (40-57 years) being compared with the highest (67-74 years). The decrease in heart rate and systolic blood pressure after intravenous metoprolol in the acute phase was similar in the elderly and the younger patients. Hypotension was observed more often in the metoprolol-treated than in the placebo-treated younger patients, while no difference was observed in the elderly. Bradycardia was observed more often in the metoprolol group in both age groups, while there was no difference regarding the incidence of congestive heart failure in either the younger or in the elderly patients. The effect on mortality, serious ventricular arrhythmias and chest pain seemed to be similar in different age groups. From the present series we conclude that hemodynamic reactions and tolerability to beta-blockade can be expected to be similar in elderly and younger patients.
Coronary sinus flow (CSF) was measured in seven patients with normal coronary arteries (group A) during intracoronary injections of 6 ml arterial blood, 6 ml blood from the coronary sinus, 3 and 6 ml isotonic saline, 3 and 6 ml hypertonic glucose, and 6 ml of a contrast agent (sodium metrizoate). In 10 patients with coronary artery disease (group B), CSF was measured after administration of 6 ml isotonic saline, 6 ml sodium metrizoate, and 6 ml of another contrast medium (iohexol). In group A, arterial blood did not affect CSF, while coronary sinus blood induced a 33% increase. After 6 ml isotonic saline, there was a 35% increase in flow and after hypertonic glucose an increase of 70%. Metrizoate induced a rise in flow of 109%. In group B, the increase in CSF after intracoronary injection of saline, metrizoate, and iohexol was 30%, 83%, and 67%, respectively. Blood from the coronary sinus, in contrast to arterial blood, induced a marked rise in peak flow, suggesting a role for reactive hyperemia secondary to myocardial hypoxia in this response. A similar mechanism might have been operative after injection of isotonic saline, as well as after the hyperosmolar contrast agents. However, additional mechanisms mediated by the high osmotic pressure of these substances, such as induction of the Bezold-Jarisch reflex, which will induce coronary vasodilation, may have played a role. Finally, when hyperosmolar agents are used, the possibility of some direct vasodilating properties of the agents cannot be excluded.
The rehabilitation of 3053 consecutive patients with femoral neck fractures from Stockholm County was followed up for 6 years. Of the patients 79 per cent were admitted from home. The majority of these patients returned home within 6 months, but patients from the city did so more slowly than patients from rural areas, and with increased secondary rehabilitation measures. Patients treated in general surgical units stayed longer and utilized more secondary rehabilitation resources than those treated in orthopaedic units. At 1 year most differences were equalized.
Different sized ROIs within the femoral head and different modes of calculation were used in [99mTc]MDP scintimetry after femoral neck fracture. In preoperative scintimetry, correction for increased trochanteric uptake gave the best discrimination, whereas in postoperative scintimetry the direct ratio fractured/intact femoral head was superior. The change in ROI size had little influence.
During the initial hospitalization, ventricular fibrillation (VF) developed in 6 metoprolol-treated patients (0.9%) vs 17 placebo-treated patients (2.4%) after inclusion in the study (p = 0.035). There were 6 episodes of VF in the metoprolol group compared with 41 episodes in the placebo group (p less than 0.001). During the same period, 14 metoprolol-treated patients had treated ventricular tachycardia vs 26 placebo-treated patients (p = 0.076). Similar favorable results were found when the incidence of severe ventricular arrhythmias during the first rehospitalization within the 3-month double-blind treatment period was analyzed.
The Göteborg Metoprolol Trial was a double-blind, placebo-controlled, stratified trial aimed at evaluating the effect of the beta 1-selective blocker, metoprolol, in suspected acute myocardial infarction and during 2 years of follow-up. The primary end-point was 3-month mortality (blind treatment period). Secondary end-points were 2-year mortality, indirect signs of infarct size, chest pain, arrhythmias and tolerability. The entry criteria were fulfilled in 2,802 patients, 1,395 of whom were included in the trial. Treatment started as soon as possible after arrival in hospital with intravenous administration followed by oral treatment for 3 months. All patients were randomized 48 hours or less after estimated onset of infarction and 69% were randomized at 12 hours or less. The blind treatment had to be withdrawn in 19% of all randomized patients before the end of the 3-month follow-up.
The effect of metoprolol on chest pain was compared with that of placebo in all randomized patients. The pain score before and 15 minutes after the injection of trial medication was registered and a reduction in chest pain was observed in the metoprolol group. Increasing chest pain after blind injection was observed in only 16 and 9 patients from the placebo and metoprolol groups, respectively. Comparison with the placebo as well as detailed analysis of clinical data revealed that in these patients the increasing pain could not be explained by coronary spasm evoked by beta-blockade. Similarly, metoprolol did not exhibit any unfavorable effect on the 14 patients who were withdrawn (together with the 28 patients given placebo) from blind treatment due to angina pectoris. Either metoprolol does not induce coronary vasospasm or spasm does not play a role in these patients with definite and suspected acute myocardial infarction as well as unstable angina pectoris. Metoprolol reduced the need for analgesics during the first 4 days and shortened the duration of pain. The effects were similar in patients with early and late treatment, but may depend on initial heart rate, blood pressure and site of infarction.
During the 3-month blind treatment period there were 40 deaths in the metoprolol group compared with 62 deaths in the placebo group (p = 0.024). During the first year (after 3 months the 2 groups were treated similarly) there were 64 deaths in the metoprolol group vs 93 in the placebo group (p = 0.017) and during 2 years 92 patients died in the metoprolol group vs 120 in the placebo group (p = 0.043). The relative incidence of different causes of death did not differ significantly between the 2 treatment groups, indicating that metoprolol reduced all causes of death to the same extent as its effect on overall mortality.
In a double-blind trial, 30 patients with suspected acute myocardial infarction with onset of symptoms within the previous 24 h were randomized to treatment with 10 mg nifedipine/placebo orally 4 times a day during hospitalization. All patients were given 15 mg metoprolol intravenously 20 min after the initial administration of nifedipine/placebo, and thereafter, 50 mg 4 times a day. The combined therapy resulted only in moderate changes in systolic blood pressure and heart rate compared with metoprolol alone. Three of the 15 patients in the nifedipine group versus 2 of the 15 in the placebo group were withdrawn because of hypotension and/or bradycardia. None was withdrawn because of congestive heart failure or A-V block. It is concluded that the combination of nifedipine and metoprolol seems to be a relatively well-tolerated combination in acute myocardial infarction.
In 585 patients having an acute myocardial infarction for the first time the relationship was investigated between estimated infarct size and the incidence of ventricular fibrillation and treated ventricular tachycardia during hospitalization. The size of the infarct was estimated from analyses of heat stable lactate dehydrogenase (LD) (EC 1.1.1.27.) in serum collected every 12 hr for 48-108 hr. All patients participated in a double-blind comparison of the beta 1-selective blocker metoprolol with placebo in suspected acute myocardial infarction. A correlation was observed between the enzymatically estimated infarct size and the incidence of ventricular fibrillation and treated ventricular tachycardia in patients on placebo (P less than 0.001), while this could not be demonstrated in patients on the beta-blocker (P greater than 0.2). In placebo treated patients there was a correlation between the maximum heat stable LD activity and early ventricular fibrillation (P = 0.034), late ventricular fibrillation (P less than 0.001), primary ventricular fibrillation (P = 0.002) as well as secondary ventricular fibrillation (P = 0.034). It is concluded that there seems to be a relatively strong correlation between the final size of the infarction and the occurrence of severe ventricular arrhythmias. Treatment with beta-blockade appeared to disturb this correlation.
Explore the source record for details and available documents.
A haemodynamic and myocardial metabolic study was performed to compare effects of maximal atrial pacing and the cold pressor test (CPT) in patients with angina pectoris. Twelve patients (group I) had angiographically severe coronary artery disease, while 16 patients (group II) had normal coronary angiograms. At maximal pacing, angina developed in all patients in group I, and myocardial lactate production was found in eight of 12 patients. In group II, 12 out of 16 patients experienced chest pain, but only two patients had myocardial lactate production. Neither angina nor myocardial lactate production was present in any patient in either group during CPT. Coronary sinus flow increased and coronary vascular resistance decreased significantly in both groups at maximal pacing (P less than 0.001). At CPT, coronary flow decreased (P less than 0.05) and coronary resistance increased (P less than 0.001) in group I, while individual response was more variable in group II. In conclusion, maximal pacing was a more effective method of provocation of angina pectoris than CPT. The reactions of coronary sinus flow and coronary vascular resistance were different in group I than in group II. However, because of the variability of response in patients with normal coronary arteries, CPT cannot be used to distinguish patients with coronary artery disease from patients with no such disease.
We have compared the effectiveness of two different mobile coronary care systems with regard to mortality from cardiac arrest (CA) outside hospital in Gothenburg, Sweden. In period 1, the mobile coronary care unit (MCCU) was part of a randomized study of the effect of an MCCU versus standard ambulances on early mortality from ischaemic heart disease. The MCCU was single, hospital based and manned by two CCU nurses and two ambulance drivers. The organization ran on workdays 08.00 a.m. to 17.00 p.m. from October, 1973 to May, 1978, corresponding to twelve months of effective time. One-year data for the MCCU have been calculated by extrapolating to a 100% allocation to the MCCU. In period 2, from November, 1980, through December, 1981, also corresponding to twelve months of effective time, the system was reorganized to a mobile intensive care unit (MICU) manned by paramedics 24 h all days of the week, and part of the time by CCU nurses. The MICU was dispatched to all suspected emergencies and the treatment capacity was defibrillation, endotracheal intubation and, part of the time, drugs. Simultaneously with the MICU, the nearest standard ambulance was dispatched and the first crew to arrive started cardiopulmonary resuscitation (CPR). Comparing the extrapolated data from period 1 with the exact data from period 2, there was an increase in period 2 of dispatches to subjects in CA due to heart disease from 59 to 181. The retrieval of subjects in ventricular fibrillation (VF) increased from 20 to 87 as a result of reduced delay times from the collapse to alarm, start of CPR and defibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)
For one year (1 September 1975-31 August 1976) an analysis was made of all deaths occurring outside hospital in the Gothenburg area (population 480 000). The total number of deaths was 1309. It was found that 675 (52%) of these deaths were caused by ischaemic heart disease (IHD), while 54 (4%) were caused by other heart diseases. The circumstances preceding death were analyzed in 363 cases representing all autopsied subjects under 75 years of age who died from IHD (autopsy rate 95%). Of these, 68% died at home, 4% during transport to hospital, and 4% at work. 214 (59%) of the deaths were witnessed, and in 189 (52%) cases, an ambulance had been called. 111 (52% died within 1 min of the onset of symptoms. 23 subject were in ventricular fibrillation on arrival at hospital. 11 of them were resuscitated, but only 3 were discharged alive. Additionally 12 of the non-autopsied subjects who died from IHD and 11 who died from other heart diseases had been witnessed and an ambulance had been called. In summary, 212 subjects who died outside hospital from heart disease in one year in Gothenburg died witnessed, and an ambulance was called. This should be the maximum annual number of cases of cardiac arrest outside hospital which it is possible to reach with a mobile coronary care organization within the time limit for effective resuscitation attempts.