Differences in the diagnosis of myocardial infarction by troponin T compared with clinical and epidemiologic criteria.

We investigated the difference in the number of myocardial infarction (MI) diagnoses based on troponin T compared with clinical and epidemiologic (modified FINnish Multinational MONItoring of trends and determinants in CArdiovascular diseases) diagnoses, and the prognosis of patients with discordant diagnoses. Five hundred fifty-nine consecutive patients (315 men and 244 women, median age 69 years) were admitted to the hospital with a suspected acute coronary syndrome. Median follow-up time was 17 months. Of the 559 patients, 127 had a clinical and 137 an epidemiologic diagnosis of MI. When a diagnosis of MI was primarily based on troponin T (>0.10 microg/L), the number of MIs was 169, which increased by 33% compared with the number of MIs by clinical diagnosis, and by 23% compared with those by epidemiologic diagnosis. However, troponin T was not elevated in 13% of the 127 patients with the clinical diagnosis and in 14% of the 137 patients with the epidemiologic diagnosis of MI. Among patients in whom clinical diagnosis of MI was not made, the prognosis with regard to coronary death or nonfatal MI was not significantly worse in patients with troponin T >0.10 microg/L than < or =0.10 microg/L (hazard ratio 1.07; 95% confidence interval 0.62 to 1.84). In patients with a suspected acute coronary syndrome, troponin T-based diagnostics leads to an increase in the number of patients diagnosed with MI compared with clinical or epidemiologic diagnosis. The prognostic impact of troponin T in patients without clinical diagnosis of MI based on elevations in conventional enzyme activities needs further study in larger series of patients.

Delays in thrombolytic therapy for acute myocardial infarction in Finland. Results of a national thrombolytic therapy delay study. Finnish Hospitals' Thrombolysis Survey Group.

OBJECTIVE: To determine lengths and causes of pre- and in-hospital delays in thrombolytic treatment. DESIGN: A prospective national survey covering 48 of the 51 Finnish university, central and general hospitals to obtain basic data before the start of a public campaign to shorten patient-related delay in acute myocardial infarction. SUBJECTS: One thousand and twelve consecutive patients with acute myocardial infarction who received thrombolytic therapy over 3 months in 1995 and who represent 40% of all patients with confirmed acute myocardial infarction. RESULTS: The median interval between onset of infarction symptoms and initiation of thrombolytic therapy was 160 min (30-647). Only 13% of the patients received thrombolysis within 60 min and 38% within 120 min. The median time from the onset of symptoms to the call for help was 60 min (5-491), and no difference was found in patients with or without a history of previous myocardial infarction (60 and 64 min, respectively). Only 52% of the patients called to the dispatch centre. The median delay from calling for help to hospital arrival was 40 min (10-170). The median in-hospital door-to-needle thrombolysis delay was 40 min (12-196). In 13% of hospitals the median delay was more than 60 min. The emergency physician encountered difficulties in decision making in 33% of cases. CONCLUSIONS: Only 38% of the patient received thrombolysis within 2 h of onset of symptoms. Patient-related delay before they sought help accounted for the major portion of the total treatment delay. Thus the findings emphasize the importance of prompt action when people are confronted with an acute heart attack. Reorganizing the emergency medical service and emergency department routines is also a necessary target to shorten thrombolysis delays. The delay attributable to transporting patients could be shortened by initiating thrombolytic treatment in the pre-hospital setting. In Finnish hospitals, door-to-needle delay was acceptable in cases with clear indications for thrombolysis. However, emergency physicians often had diagnostic difficulties, which led to remarkably longer in-hospital delays.

Comparison of sotalol with digoxin-quinidine for conversion of acute atrial fibrillation to sinus rhythm (the Sotalol-Digoxin-Quinidine Trial).

We randomized 61 patients with paroxysmal atrial fibrillation (AF) ( < 48 hours from onset) to either sotalol or quinidine treatment. Conversion of rhythm was recorded by Holter monitoring. The starting 80 mg dose of sotalol was repeated at 2, 6, and 10 hours if AF persisted (heart rate > 80 beats/min), and if systolic blood was > or = 120 mm Hg. In the quinidine group, if heart rate > 100 beats/min, it was decreased with intravenous digoxin, whereafter 200 mg of oral quinidine sulfate was given maximally 3 times, each dose 2 hours apart. Conversion of AF to sinus rhythm occurred in 17 or 33 patients (52%) taking sotalol, and in 24 of 28 patients (86%) taking quinidine (p < 0.0001). Electric cardioversion was necessary in 39% of the former and in 14% of the latter group. The mean delay from first trial drug to sinus rhythm with the trial medication was 10.2 +/- 7.6 hours in the sotalol group and 4.0 +/- 2.9 hours in the quinidine group (p < 0.01). Treatment was discontinued in 16 patients taking sotalol (48%) because of asymptomatic bradycardia or hypotension, and in 20 taking quinidine (71%) because of rhythm conversion. Asymptomatic wide complex tachycardia (QRS > 0.12 second) was found in 13% and 27% of patients taking sotalol and quinidine, respectively. The longest RR intervals were 6.4 and 3.8 seconds in the sotalol and quinidine groups, respectively. Oral sotalol did not appear as effective as quinidine sulfate treatment in conversion of paroxysmal AF.(ABSTRACT TRUNCATED AT 250 WORDS)

Fatal road accidents caused by sudden death of the driver in Finland and Vaud, Switzerland.

We investigated the incidence of fatal traffic accidents caused by sudden incapacity of the driver due to cardiac and other illnesses. The retrospective analysis was gleaned from Finnish traffic accident data files from 1984-1989, and police records of traffic accidents, from Canton de Vaud, Switzerland from 1986-1989. The annual rates of all traffic fatalities per million inhabitants were 125 in Finland and 212 in Vaud. Sudden driver incapacity due to acute illness caused 1.8 and 7.3 automobile driver deaths annually per million inhabitants in Finland and in Vaud, respectively. The corresponding rates for all-cause traffic deaths were 326 and 423, for driver deaths 105 and 167, and for those due to driver incapacity 4.7 and 15.6. Sudden driver incapacity caused 1.5% of all traffic deaths in Finland, and 3.4% in Vaud. Probable cardiac arrest caused 2.1% of all drivers' deaths in Finland and 1.7% in Vaud, respectively. Deaths caused by professional drivers' sudden incapacity were responsible for 0.11% of all traffic deaths in Finland, and for 0% in Vaud. Old age and short mileage were associated with illness-caused accidents. Accidents caused by sudden incapacity of the driver are rare causes of traffic deaths and hard to foresee. While this report relates to all drivers, we suggest there should be individual risk stratification for professional drivers with heart disease. However, non-professional drivers who are elderly and who have symptomatic cardiac disease should limit their driving to short distances and at low speed.

Morphometric study of human myocardium in acquired valvular diseases.

To study the effect of various valvular heart diseases on the quantitative histology of myocardium, 38 human hearts with valvular lesions were examined (11 aortic stenoses, nine mitral stenoses, nine mitral incompetence and nine combined aortic and mitral valve lesions). The control group consisted of ten hearts without any valvular lesions. With morphometrical methods the volume fractions of myocardial components (myocardial fibres, interstitial space and diffuse connective tissue), the numerical density of arterioles and the mean fibre diameter were estimated. Myocardial fibrosis was more severe in hearts with valvular lesions than in the controls (5.4% vs 3.3%, P less than 0.01), but did not correlate with the anatomical severity of the valvular lesions. The most severe myocardial fibrosis was found in hearts with mitral incompetence (6.7%). Fibre hypertrophy was most severe in hearts with aortic stenosis and in hearts with mitral incompetence (22 microns and 23 microns, respectively). In hearts with severe valvular lesions the mean fibre diameter was 23 microns and in hearts with mild to moderate lesions 19 microns (P less than 0.01). Good correlation was observed between the mean fibre diameter and the weight of the left ventricle (r = 0.81, P less than 0.01). The volume fractions of connective tissue and interstitial space were significantly higher and the volume fraction of myocardial fibres was correspondingly lower in the subendocardium than in the subepicardium in hearts with either pressure overload (aortic stenosis) or volume overload (mitral incompetence). In conclusion, myocardial fibrosis occurs in patients with various valvular lesions, but the severity of the fibrosis does not correlate with the anatomical severity of valvular lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of early metoprolol injection followed by oral dosage on CK-MB release, and myocardial function in suspected acute myocardial infarction. A double-blind controlled study.

The effect of metoprolol on indices of infarct size and left ventricular function was compared with that of placebo in a double-blind randomized trial in patients with definite or suspected acute myocardial infarction. Intravenous metoprolol (15 mg) or placebo was given within 24 h of the onset of symptoms, and oral treatment (200 mg daily) was continued for 15 days. Thirty-five patients received metoprolol and 34 patients placebo. The mean (+/- SD) of maximal creatinine phosphokinase (CK)-MB activities was 142 +/- 110 IU/l in the placebo group and 74 +/- 72 IU/l in the metoprolol group (p less than 0.001). The ECG QRS score at discharge from hospital was 5.22 +/- 4.47 and 4.61 +/- 3.06 (NS), respectively. Global left ventricular ejection fraction at rest was 44 +/- 14 and 51 +/- 15% (p = 0.054), respectively, and no change occurred in either group from rest to peak exercise. Ventricular fibrillation occurred in 1 placebo patient during the first day in hospital and in 1 metoprolol patient on the 14th day. Holter monitoring revealed no significant difference in the occurrence of ventricular arrhythmias during the first 24 h. Smaller enzyme release and higher ejection fraction suggest myocardial protection by early metoprolol treatment in acute myocardial infarction.

Changes occurring in the postinfarction ECG in relation to age, sex, and previous myocardial infarction.

Minnesota codes (MC), expressing Q-QS, ST segment, and T wave abnormalities in ECGs taken during the acute event and at a 1-year follow-up were studied in 256 survivors of myocardial infarction (MI). On the 1-year ECGs large Q waves (MC 1.1) were more common in patients with a history of previous MI than in those with a first MI. Regression of Q-QS, ST segment, and T wave changes occurred more extensively in first MIs, whereas progression of MC Q-QS and ST segment signs tended to be common in those with recurrent MI. On the acute ECGs large Q waves were more frequent in men (52%) than in women (36%), but ST segment depression of 1 mm or more (MC 4.1) was predominant in women in both the acute and 1-year ECGs. This ECG sign was related to the advanced age of the patients. There was no significant sex difference in the regression of the Q-QS signs, but the disappearance of ST and T wave changes occurred more extensively in men. The ECG returned to normal in 12% of men with a first MI but only infrequently in women and men with recurrent MI.

Enalapril in chronic heart failure, a double-blind placebo-controlled study.

The efficacy of enalapril, a new angiotensin-converting enzyme inhibitor, was investigated in a double-blind placebo-controlled study in 24 patients with chronic heart failure. The patients belonging to NYHA functional class II-IV and treated with digoxin and diuretics were randomized to enalapril (12 patients) or placebo (12 patients) treatment for a 12-week period. Assessments were carried out at baseline and at 4 and 12 weeks during the treatment period. Complete data could be obtained on 10 patients receiving enalapril and on 11 patients receiving placebo. NYHA functional class improved by at least one class in 6 of 10 patients in the enalapril group, but only in 1 of 11 patients in the placebo group (chi 2 = 6.54; p less than 0.05). Duration of bicycle ergometer exercise increased significantly in the enalapril group from 8.8 +/- 3.4 to 11.3 +/- 4.2 (4 weeks) and to 11.2 +/- 3.6 min (12 weeks; p less than 0.05 for both), whereas it remained unchanged in the placebo group. Left ventricular ejection fraction by radionuclide ventriculography in the enalapril group increased significantly (baseline: 33.5 +/- 19.9%, 4 weeks: 40.0 +/- 20.0% (p less than 0.001), 12 weeks: 39.6 +/- 20.1% (p less than 0.01], whereas in the placebo group it did not change significantly from the baseline of 48.8 +/- 16.7%. The results indicate that enalapril induces a sustained relief of symptoms and improves exercise capacity in patients with heart failure. This subjective improvement appears to be accompanied by an increase in ejection fraction.

Cirrhosis of the liver markedly impairs the elimination of mexiletine.

To study the effects of cirrhosis of the liver on the pharmacokinetics of mexiletine a single i.v. dose of 200 mg was administered to six cirrhotic patients and to six healthy controls. The distribution of mexiletine in both study groups was similar, as indicated by similar values of V1 and Vss, but it tended to occur more slowly in the cirrhotics. The plasma protein binding of mexiletine was unchanged in the patients with cirrhosis. The elimination of mexiletine was markedly retarded in the cirrhotics, as indicated by its lower total clearance (2.31 vs. 8.27 ml/kg/h,) lower total elimination rate constant (0.059 vs 0.353 h-1), and longer elimination half-life (28.7 vs 9.9 h). The antipyrine half-life was 38.3 h in the patients and 14.7 h in the controls. One healthy volunteer had a Morgagni-Stokes-Adams type of syncopal attack 5 min after administration of mexiletine due to disturbance of AV conduction induced by the drug. Thus, on a pharmacokinetic basis the loading dose of mexiletine need not be modified in cirrhotic patients, whereas the maintenance dosage should be reduced to one fourth - one third of the usual dose.