Mutations in the gene for cardiac myosin-binding protein C and late-onset familial hypertrophic cardiomyopathy.

BACKGROUND: Mutations in the gene for cardiac myosin-binding protein C account for approximately 15 percent of cases of familial hypertrophic cardiomyopathy. The spectrum of disease-causing mutations and the associated clinical features of these gene defects are unknown. METHODS: DNA sequences encoding cardiac myosin-binding protein C were determined in unrelated patients with familial hypertrophic cardiomyopathy. Mutations were found in 16 probands, who had 574 family members at risk of inheriting these defects. The genotypes of these family members were determined, and the clinical status of 212 family members with mutations in the gene for cardiac myosin-binding protein C was assessed. RESULTS: Twelve novel mutations were identified in probands from 16 families. Four were missense mutations; eight defects (insertions, deletions, and splice mutations) were predicted to truncate cardiac myosin-binding protein C. The clinical expression of either missense or truncation mutations was similar to that observed for other genetic causes of hypertrophic cardiomyopathy, but the age at onset of the disease differed markedly. Only 58 percent of adults under the age of 50 years who had a mutation in the cardiac myosin-binding protein C gene (68 of 117 patients) had cardiac hypertrophy; disease penetrance remained incomplete through the age of 60 years. Survival was generally better than that observed among patients with hypertrophic cardiomyopathy caused by other mutations in the genes for sarcomere proteins. Most deaths due to cardiac causes in these families occurred suddenly. CONCLUSIONS: The clinical expression of mutations in the gene for cardiac myosin-binding protein C is often delayed until middle age or old age. Delayed expression of cardiac hypertrophy and a favorable clinical course may hinder recognition of the heritable nature of mutations in the cardiac myosin-binding protein C gene. Clinical screening in adult life may be warranted for members of families characterized by hypertrophic cardiomyopathy.

[A prospective study of oral anticoagulation therapy monitored with the P&P-test.].

OBJECTIVE: To analyze the outcome of patients on oral anticoagulation therapy who are monitored with the prothrombin proconvertin time (P&P-test, PP). MATERIAL AND METHODS: The prothrombin-proconvertin time was used to adjust anticoagulant intensity in a prospective study of 326 patients treated with oral anticoagulants for a study period of 121 patient years. The goal intensity INR was 2.0-3.0 for all patients. The main indications were: artificial heart valves 26%, venousthromboembolism 25%, atrial fibrillation 23%, atherosclerotic disease 14% and systemic arterial embolism of uncertain etiology 7%. RESULTS: INR calculated directly from the PP correlated well with INR calculated from the PT. The mean time adjusted anticoagulant intensity was 2.3 and did not differ significantly according to indication. Six major bleedings, including one fatal, occurred in five patients during the study period. The INR was 1.8 in one patient who bled from a duodenal ulcer, but 6.8,7.9,8.6,11.6 (died) and 15.5 at five other events. The INR was <4.5 during 97% of the treatment time of the whole group and 1% of treat notment time were at an INR>6.0. The bleeders had a different pattern with 18% of the treatment time at INR>6.0. The risk of bleeding was one for every 73 days at that intensity or an almost 600 fold risk increase compared to an INR<4.5. One patient anticoagulated for systemic embolism had cerebral infarction with an event related INR of 2.0. Two patients with atrial fibrillation died from acute myocardial infarction but event related INR's were not available. One patient anticoagulated for venous thromboembolism died suddenly but was not autopsied. No embolic events occurred in patients with artificial heart valves in spite of the low intensity anticoagulation. CONCLUSION: Despite a relatively low intensity in all patient groups in this study thromboembolic events were rare. The risk of bleeding increased markedly at INR>6.0. The mortality rate of the ariticoagulated population was comparable to the expected age adjusted Icelandic mortality rate.

Performance of prothrombin-proconvertin time as a monitoring test of oral anticoagulation therapy.

Outcome and anticoagulation intensity was evaluated during 121 patient years of oral anticoagulant therapy monitored with the prothrombin-proconvertin clotting time (PP, also known as P&P). The PP-based international normalized ratio (INR; PP-INR) correlated well with the INR calculated from the prothrombin clotting time (PT; r = 0.92), and results were almost identical over a wide range after linear conversion (1/INR). When the PP-INR was 4.5 or less, the risk of major bleeding was 1 for every 118 treatment years, but it was 1 for every 73 days when the INR was 6 or more. The 1/PP-INR correlated better with factor II coagulant activity (r = 0.85) than did the 1/PT-INR (r = 0.78). The 1/PP-INR also correlated better with the native prothrombin antigen (r = 0.76) than did the 1/PT-INR (r = 0.68). The PP and PT results correlated better with factor II coagulant activity than with native prothrombin antigen. Thus, the PP clotting time results can be accurately converted to INR. The results also suggest that the PP may have advantages over the PT as an indicator of anticoagulation intensity during oral anticoagulation.

[A left main coronary artery arising from the pulmonary artery. Case report.].

Anomalous origin of the left coronary artery from the pulmonary artery is a rare congenitial heart disease. Most patients are diagnosed shortly after birth but occasionally the anomaly is diagnosed in teenagers or adults. Prognos is dismal without operation. We describe the first case diagnosed and treated in Iceland. The patient, an asymptomatic 14 year old boy, underwent both the socalled Takeuchi's tunnel plastic and a coronary bypass operation.

Fosinopril versus enalapril in the treatment of hypertension: a double-blind study in 195 patients.

The new angiotensin-converting enzyme (ACE) inhibitor fosinopril was compared with the ACE inhibitor enalapril in a multicenter (n = 11), multinational (Denmark, Finland, Iceland, Norway, and Sweden), double-blind, randomized, parallel-group 24-week study in 195 patients with mild to moderate essential hypertension [supine diastolic blood pressure, (SDBP) > or = 95 to < or = 110 mm Hg]. After discontinuing all previous antihypertensive medication, patients were entered into a placebo lead-in period of 4-6 weeks, followed by 24 weeks of randomized treatment with the active compounds administered with a double-dummy technique. The dose of fosinopril was 20 mg, which could be increased to 40 mg after 8 weeks (average 25.6 mg); that of enalapril was 10 mg, which could be increased to 20 mg after 8 weeks (average 12.9 mg). Hydrochlorothiazide 12.5 mg could be added after 16 weeks and was administered to 27% of the patients in the fosinopril group and to 30% in the enalapril group. All drugs were administered once daily. Supine systolic BP (SSBP) decreased from 157 to 143 mm Hg in the fosinopril group (p < 0.01), and from 159 to 147 mm Hg in the enalapril group (p < 0.01). SSDP decreased from 100 to 89 mm Hg in the fosinopril group (p < 0.01) and from 100 to 92 mm Hg in the enalapril group (p < 0.01). Throughout the study period, fosinopril reduced SSBP and SDBP numerically more than did enalapril, by 0-3 mm Hg. Adverse events (AE) caused withdrawal of study medication in 8 patients in the fosinopril group and in 14 patients in the enalapril group (NS). The number of reported AE was not statistically different in the two groups. Inhibition of the ACE was assessed in a subgroup of patients (n = 26, 13 in each group). Fosinopril caused a greater inhibition of ACE at the doses used in the present study, which was statistically significant. Both fosinopril and enalapril caused statistically significant reductions in BP of a similar magnitude, and both agents were well tolerated. However, fosinopril was consistently numerically slightly more effective than enalapril in reducing BP. There were fewer withdrawals due to AE (NS) in the fosinopril group, and the overall recorded AE were fewer in the fosinopril group (NS).

[Blood pressure at the clinic, work and home. Are there white coats at work?].

BACKGROUND: Today there are mainly three methods for measuring blood pressure, namely by a health worker at the clinic, by self-monitoring (often called home monitoring) and ambulatory monitoring. These methods give different mean values. All present studies concerning the relation between high blood pressure and organ damage are based on blood pressure measurements at clinics, and therefore the predictive values of home and average 24-h ambulatory measurements are not known. Comparative studies on "white coat effect" on blood pressure in Iceland are lacking. Furthermore, the Icelandic people have long working days and therefore some knowledge on blood pressure at work is of interest. The relation between blood pressure at the clinic and at work is unknown Objective: To analyse possible white coat effects of blood pressure and to compare these measurements with blood pressure values at work. MATERIAL AND METHODS: During 1993-1994, 84 males aged 25-65 years were allocated to the study from five health centres and two hypertension clinics. Self-measurements of blood pressure were performed on UA-751 Digital Blood pressure Meter at home, at work and at the clinic. All measurements were scheduled between 3 and 5 PM. For comparison with blood pressure at the clinical setting, the pressure was also measured by the doctor using conventional mercury sphygmomanometer. Three measurements were recorded at each place but only one each day. RESULTS: Good correlation was found between mercury sphygmomanometer and automatic meter measured at the clinic when measured by standard correlation coefficients (r=0.9; p<0.001). Agreement analysis demonstrates however, more discrepancy between these two methods. Mean blood pressure is similar at the clinic and at work, but significantly higher than mean blood pressure at home (p<0.001 for both systolic blood pressure and diastolic blood pressure). Possible white coat (15%) and work related (12%) hypertension was observed. CONCLUSION: The mean blood pressure at work and in the clinic is similar and higher than that recorded at home. This strengthens the predictive value of clinical measurements and demonstrates the rise of blood pressure outside the home is not only due to a white coat effect. Self measurements at home can be useful to detect white coat phenomena. Comparison of self-measurements at work and at home can perhaps help to detect these effects. The agreement between the automatic blood pressure meter and the conventional mercury sphygmomanometer is unsatisfactory for clinical purposes and therefore the methods are not interchangeable.

[Cardiac surgery because of congenital heart disease on Icelandic children born 1969-1993.].

The incidence of congenital heart disease (CHD) has been shown to be 0.8-1.0% and of these 0.5% will require specific treatment. An investigation on Icelandic children born 1985-1989 showed a slightly higher incidence or 1.1%. Iceland is well suited for population studies because investigation, treatment or treatment decision are made centrally, the population is stable and the country geographically well defined. The purpose of our study was to investigate the number of Icelandic children who required cardiac surgery because of CHD, the distribution between specific defects, the number of operations, age at first operation, mortality and causes of death. The study deals with children born in Iceland from 1969 to 1993 that had been operated upon for CHD during the period January 1st 1969 to May 1st 1994. Data were collected from the Departments of Pediatrics, Surgery and Medicine of Landspitalinn, National University Hospital. During this 25 year period 299 children had 354 operations because of CHD or 2.75 per 1000 livebirths. The mean age at operation has fallen from 4.7 years in 1969-1973 to 0.8 years in 1989-1993. Operations done in England were 261 and 79 in Iceland. The most commonly encountered defect was ventricular septal defect (VSD). During the study period the frequency of operations for the individual defects was stable except for atrial septal defect (ASD) which increased after 1984. Of the 299 children 31 are dead (10.4%). Of 1000 live born children 2.75 will require cardiac surgery because of CHD. The reason for reduced age at operation and increasing operation frequency for ASD are probably because of better diagnostic technique and improved knowledge about the disease process.

[The optimal combination of captopril and hydrochlorothiazide in mild hypertension.].

OBJECTIVE: We have previously shown that in the treatment of mild to moderate hypertension little is gained by increasing the dose of hydrochlorothiazide (HCT) over 12.5 mg when combined with an ACE-inhibitor. An increase in dosing was associated with more numerous side effects. The present study was designed to explore the relative efficacy of 12.5 and 6.25 mg of HCT in combination with captopril (C). MATERIAL AND METHODS: For the study 25 patients with mild hypertension were recruited. Their mean age was 63 years (SD +/- 13 years). After a four week wash-out period and a dose finding phase of eight weeks, eight patients were stabilised at a diastolic pressure of <95 mmHg on C 50 mg + HCT 12.5 mg and 17 on C 25 mg + HCT 12.5 mg. These doses of C were continued throughout the study. The patients were then divided in two groups, receiving 12.5 mg or 6.25 mg of HCT for four weeks. The groups were then crossed over and treated for a further four week period. Finally, placebo was given for HCT for four weeks. RESULTS: Although the mean supine blood pressure was lower on HCT 6.25 mg than placebo by 5/3 mmHg this difference was not significant. The pressure fall on HCT 12.5 mg in comparison with placebo was significant (9/7 mmHg, p<0.02) and the supine systolic blood pressure was similarly significantly lower on HCT 12.5 mg than 6.25 mg (p<0.02). The mean serum-K was significantly reduced by HCT 12.5 mg but only two patients had values below 3.5 mmol/1 and none below 3.0 mmol/1. No change was observed in serum creatinine values. No significant increase was reported in side effects on HCT + C in comparison with placebo + C. CONCLUSION: This and our previous studies suggest an optimal dose of HCT of approximately 12.5 mg. A dose of 6.25 mg may not be without an antihypertensive effect. However, such an effect is likely to be modest.

Acute myocardial infarction in the young--the role of smoking. The Investigators of the International Tissue Plasminogen Activator/Streptokinase Mortality Trial.

Patients who received thrombolytic therapy for acute myocardial infarction in a large international trial were divided into two groups on the basis of age; those < or = 40 years (n = 269) and those > 40 years (n = 7787). The younger group included more men (89.9% vs 75.9%, P = 0.009) and fewer patients had a history of coronary artery disease, hypertension, and diabetes mellitus. A family history of cardiovascular disease was significantly more prevalent among the young patients (53.4% vs 41.9%, P = 0.0002). Significantly more younger patients than older patients were smokers at the time of infarction (76.2% vs 42.9%, P < 0.0001) and the average number of cigarettes smoked per day was also significantly higher in young patients (27.8 +/- 14.3 vs 19.9 +/- 12.9, P < 0.01). Younger patients had a better outcome, with lower rates of cardiogenic shock (1.1% vs 7.0%, P = 0.0002), stroke (0.0% vs 1.9%, P = 0.02) and haemorrhage (1.9% vs 5.9%, P = 0.006), as well as a better Killip class at discharge (Killip > 1 in 4.5% vs 8.0%, P < 0.001), and lower hospital and 6-month mortality (0.7% and 3.1% vs 8.3% and 12%, P < 0.001, respectively). The better outcome of younger patients with acute myocardial infarction is related to their better baseline characteristics. Young patients with acute myocardial infarction have a strong family history of cardiovascular disease and a high prevalence of smoking. Smoking is the most important modifiable risk factor in these patients.

Outcome of thrombolytic therapy in relation to hospital size and invasive cardiac services. The Investigators of the International Tissue Plasminogen Activator/Streptokinase Mortality Trial.

OBJECTIVE: The outcome of patients with acute myocardial infarction who received thrombolytic therapy was assessed in relation to the size and comprehensiveness of cardiovascular services in the admitting hospitals. METHODS: Two characteristics were obtained for each of the 438 hospitals: number of beds and in-house availability of cardiovascular services (coronary catheterization laboratory and coronary angioplasty or bypass surgery). Hospitals were grouped into four categories on the basis of size (< or = 300 vs > 300 beds) and availability of cardiovascular services. Baseline and outcome variables were compared by chi 2 analysis and logistic regression. Patients were followed up for 6 months. RESULTS: Baseline variables were comparable among hospital categories except for significant differences in the distribution of antecedent angina and time to treatment. Significantly more coronary angioplasties and bypass surgeries were performed in patients first treated in hospitals with coronary revascularization services (4.1% and 4.2% vs 1.0% and 1.9%, P < .0001). Rates of strokes (1.9% vs 1.3% and 1.6%, P = .54), hospital mortality (11.9% vs 8.5%, (P = .11), and 6-month mortality (17.0% vs 11.8% and 12.3%, P = .03) were highest among patients treated in small hospitals that had coronary revascularization facilities. The rate of invasive procedures was higher in the smaller hospitals (odds ratio [OR], 1.44; 95% confidence limits [CL], 1.11 and 1.87; P = .006) and in hospitals with coronary revascularization services (OR, 4.05; 95% CL, 3.14 and 5.22; P < .0001); hemorrhage was more frequent in centers with coronary revascularization facilities (OR, 1.39; 95% CL, 1.13 and 1.71; P = .002). Rates of hospital mortality and 6-month mortality were similar. CONCLUSIONS: Patients with acute myocardial infarction treated with thrombolytic therapy have the same mortality in small centers without in-house coronary revascularization services as in larger centers with such services.

After correcting for worse baseline characteristics, women treated with thrombolytic therapy for acute myocardial infarction have the same mortality and morbidity as men except for a higher incidence of hemorrhagic stroke. The Investigators of the International Tissue Plasminogen Activator/Streptokinase Mortality Study.

BACKGROUND: In the prethrombolytic era, women with myocardial infarction were reported to have a worse outcome than men. This analysis evaluates the association of sex with morbidity and mortality after thrombolytic therapy. METHODS AND RESULTS: Data were analyzed from 8261 of the 8387 randomized patients with acute myocardial infarction who received thrombolytic therapy in the International Tissue Plasminogen Activator/Streptokinase Mortality Study (baseline data were missing for 126 patients) and were followed for 6 months. Women made up 23% (n = 1944) of the study population. Baseline characteristics were worse in women: they were 6 years older, were more likely to have a history of previous infarction (P < .01), antecedent angina (P < .01), hypertension (P < .0001), or diabetes (P < .0001); were in a higher Killip class on admission (P < .0002); and received thrombolytic therapy 18 minutes later than men (P < .0001). Fewer women were smokers (P < .0001). Women had a higher hospital (12.1% versus 7.2%, P < .0001) and 6-month mortality (16.6% versus 10.4%, P < .0001) and were more likely to develop cardiogenic shock (9.1% versus 6.3%, P < .0001), bleeding (7.2% versus 5.3%, P < .01), and hemorrhagic (1% versus 0.3%, P < .001) or total stroke (2.2% versus 1.1%, P < .0001) during hospitalization. Reinfarction rates and requirement for angioplasty or surgery did not differ. After correction for worse baseline characteristics, women had similar morbidity and mortality apart from a significantly higher incidence of hemorrhagic stroke, which remained significant even after accounting for weight and treatment allocation (odds ratio, 2.90; P < .01). CONCLUSIONS: After thrombolytic therapy for acute myocardial infarction, women have similar morbidity and mortality to men but suffer from a higher incidence of hemorrhagic stroke.

Significance of smoking in patients receiving thrombolytic therapy for acute myocardial infarction. Experience gleaned from the International Tissue Plasminogen Activator/Streptokinase Mortality Trial.

BACKGROUND: Despite the fact that smoking is a well-established risk factor for the development of coronary artery disease, some investigators have noted that hospital mortality after acute myocardial infarction is lower in patients who smoke than in nonsmoking patients. To evaluate the association of smoking with mortality during hospitalization after thrombolytic therapy and 6 months afterward, we analyzed the results of the International Tissue Plasminogen Activator/Streptokinase Mortality Trial. METHODS AND RESULTS: Patients were divided into three groups: nonsmokers (those who never smoked), ex-smokers, and active smokers. Multivariate and univariate comparisons were made with respect to baseline characteristics and clinical outcome. There were 2,366 nonsmokers, 2,244 ex-smokers, and 3,649 active smokers. The baseline characteristics of nonsmoking patients differed significantly from the ex-smokers and active smokers. The nonsmoking group included more women than the ex-smokers or active smokers (45% versus 10.6% and 17.6%, respectively), was older (67 +/- 10 years versus 64 +/- 10 years and 58 +/- 11 years), had a higher rate of diabetes mellitus (16.3% versus 11.1% and 7.5%), and had a worse Killip class at admission. Nonsmoking patients and ex-smokers experienced more in-hospital reinfarction than active smokers (4.7% and 5% versus 2.7%, p < 0.0001, respectively). Nonsmokers experienced more in-hospital shock than the ex-smokers or active smokers (9.2% versus 6.4% and 5.8%, p < 0.0001), stroke (1.9% versus 1.8% and 0.8%, p < 0.0001), and bleeding (7.2% versus 6.5% and 4.4%, p < 0.0001). They also experienced a higher in-hospital and 6-month mortality (12.8% and 17.6%) than ex-smokers (8.2% and 12.1%) or active smokers (5.4% and 7.8%) (p < 0.0001). A multivariate analysis accounting for all baseline characteristics demonstrated a significant association between nonsmoking and increased hospital mortality, with an odds ratio of 1.42 (confidence limits, 1.15-1.72). Among active smokers, there was a nonsignificant trend for mortality rates to decrease with increasing numbers of cigarettes smoked per day. CONCLUSIONS: This retrospective analysis indicates that smokers receiving thrombolytic therapy after acute myocardial infarction have significantly better hospital and 6-month outcome than nonsmokers or ex-smokers. However, smokers sustained their infarction at a significantly earlier age than nonsmokers, and strenuous efforts should continue to be made to decrease the incidence of new and continued smoking.

Influence of dietary cod liver oil on fatty acid composition of plasma lipids in human male subjects after myocardial infarction.

A randomized crossover study was carried out to investigate the fatty acid profile and concentrations of plasma lipids in male patients with myocardial infarction (MI) who supplemented their diet with 20 ml cod liver oil daily for 6 weeks. Subjects were divided into two groups, A and B. Group A received cod liver oil daily for 6 weeks after hospital discharge, but none for the subsequent 6 weeks. Group B did not start taking cod liver oil until 6 weeks after hospital discharge, and they then took cod liver oil for 6 weeks. Diet, medication or smoking habits were kept as constant as possible during the study. During the period of cod liver oil intake, eicosapentaenoic acid (20:5 (n-3), EPA) and docosahexaenoic acid (22:6 (n-3), DHA) increased significantly in phospholipids (PL), triglycerides (TG) and cholesterol esters (CE), whereas linoleic acid (18:2 (n-6), LA), dihomo-gamma-linolenic acid (20:3 (n-6), DHGLA) and arachidonic acid (20:4 (n-6), AA) were significantly decreased in phospholipids. The plasma level of TG was significantly decreased during the cod liver oil intake. Total cholesterol, high density lipoprotein (HDL) cholesterol, and levels of apolipoproteins A1 and B were not affected by cod liver oil in these MI patients.

Cod liver oil does not reduce ventricular extrasystoles after myocardial infarction.

Previous work has shown that in experimental animal models a lower incidence of arrhythmias and sudden death was observed if the animals were fed cod liver oil or fish oil. After a 48-h control period starting, on average, 8 days after the onset of symptoms, 18 men who were recovering from acute myocardial infarction were given 20 ml d-1 cod liver oil for 6 weeks, either immediately after the control period, weeks 0-6 (n = 10), or during weeks 6-12 (n = 8). Forty-eight-hour Holter monitoring was carried out before cod liver oil administration and at the end of weeks 6 and 12. The eicosapentaenoic acid content of plasma phospholipids was increased by 230% during cod liver oil administration. However, no significant change was observed in the 24-h prevalence of ventricular extrasystoles or other arrhythmias during the study period. The mean ln number of ventricular extrasystoles was 2.95 +/- 0.51 (+/- SEM) during cod liver oil ingestion and 2.63 +/- 0.30 when not taking cod liver oil.

Additive effects of moderate dietary salt reduction and captopril in hypertension.

In a randomized, cross-over study 27 patients had diastolic blood pressure of greater than or equal to 96 mmHg during four visits without treatment. Following captopril 25 mg b.i.d. nine patients' blood pressure was less than or equal to 90 mmHg. The remaining 18 were randomized into two treatment modalities, captopril and moderate dietary salt reduction, and captopril and hydrochlorothiazide 25 mg daily. Following a wash-out period the groups crossed over to the alternative treatment. At the end of the control period the average blood pressure was 151/100 +/- 12/6 mmHg recumbent and 140/91 +/- 11/7 standing, following captopril 144/94 +/- 13/5 and 132/92 +/- 12/6, respectively, with low salt diet added to captopril 140/91 +/- 12/6 and 128/89 +/- 11/6 and with hydrochlorothiazide and captopril 133/86 +/- 12/7 and 120/84 +/- 11/7 mmHg supine and erect, respectively. It is concluded that moderate dietary salt reduction, which is easily advised, will significantly potentiate the blood pressure fall following captopril treatment in moderate arterial hypertension.

Painful autoimmune thyroiditis occurring on amiodarone therapy.

A 51-year-old housewife, who had been on treatment with amiodarone for ten months, developed a painful enlargement of the thyroid gland. Thyroid antibody titers were highly elevated and a fine needle aspirate of the gland showed infiltration of lymphocytes and plasma cells. Initially the patient was hyperthyroid, later she developed hyperthyroidism which required thyroid substitution. The possibility of amiodarone provoking autoimmune thyroiditis is discussed.

Programmed atrial pacing for orthostatic hypotension.

Programmable atrial inhibited pacemakers were implanted in two patients with orthostatic hypotension due to autonomic failure. They were paced at 95 beats/min during the day and programmed themselves to 55 beats at night. This treatment resulted in virtual disappearance of orthostatic symptoms during a two-year follow-up. Haemodynamic studies showed a mean increase in erect systolic blood pressure from 47 mmHg pre-implantation to 85 mmHg at nine months post-implant during pacing. Cardiac output averaged 3.0 l/min without pacing and 3.8 l/min with pacing at two investigations. Rapid heart rate and high supine blood pressure at night were avoided by programming the pacemaker.

Long-term follow-up of direct current cardioversion after cardiac surgery with special reference to quinidine.

The results of the long-term follow-up of 119 patients who had DC cardioversion performed are described. All patients had had corrective cardiac surgery for chronic rheumatic valvar heart disease. The poor prognosis for maintenance of sinus rhythm in this type of patient is emphasized. Of the total patients, 83 per cent were converted to sinus rhythm, but relapses were common in those who had atrial fibrillation before operation. Only 40 per cent of such patients maintained sinus rhythm for 2 months, 15 per cent for 1 year, and 9 per cent for 2 years.By contrast, when atrial fibrillation occurred for the first time in the post-operative period, 82 per cent maintained sinus rhythm for 2 years after conversion.Post-operative DC cardioversion is in general not recommended for patients with rheumatic heart disease and atrial fibrillation unless atrial fibrillation occurs for the first time in the post-operative period. A controlled trial of prophylactic quinidine is reported and shows no significant increase in the number of patients remaining in sinus rhythm as compared with a control group not receiving quinidine.