Is smoking in pregnancy interrelated between generations?

In order to compare pregnancy smoking habits in two generations, data on first generation deliveries in 1964-67 were obtained from prospective questionnaires. By record linkage with the Swedish Medical Birth Registry, data on daughters giving second generation births (n = 1659) were obtained, including prospective smoking information. The catchment area was that of Helsingborg County Hospital (population 145,000). Second generation births until December 31, 1993 were identified in all of Sweden. The odds ratio of maternal smoking in the first generation for pregnancy smoking among the daughters was significantly increased and approximately doubled. Adjustment for confounders was made using the Mantel-Haenszel method. Similar odds ratios remained after stratification either for a social environment index of the first generation or the educational level of the second generation. Thus, our data suggest a biological association between pregnancy smoking habits over generations. Research on causative mechanisms could help design more efficient intervention programs. In a separate analysis of two parturient cohorts in Helsingborg 30 y apart, we found that the prevalence of maternal smoking had decreased comparatively more among younger than older women.

Non-invasive recognition of arrhythmogenic right ventricular dysplasia.

Arrhythmogenic right ventricular dysplasia causes ventricular arrhythmias and sometimes heart failure. The condition is easily overlooked, but once suspected, it may be diagnosed non-invasively. This is illustrated by the case reported. The clinical features of this syndrome are discussed, with special emphasis on the non-invasive findings.

Serum LD-1 activity in suspected acute myocardial infarction.

We have studied the diagnostic value of measuring lactate dehydrogenase (LD) isoenzyme 1 in serum of 331 cases of suspected acute myocardial infarction (AMI). At a discriminatory level of 200 U/L (Scandinavian Committee on Enzymes, recommended method for the determination of LD) LD 1 verified the diagnosis in 96% of the AMI cases and excluded it in 96% of the not-AMI cases when samples were drawn 24-72 h after onset of pain. The correlation between 24-h S-LD-1 and 16-h S-CK B activities was 0.94 in the AMI cases. We found that quantitation of serum LD-1 is diagnostically more reliable than the serum LD-1/LD ratio.

Creatine kinase and creatine kinase B-subunit activity in serum in cases of suspected myocardial infarction.

We evaluated a diagnostic strategy by studying 481 patients suspected of having had an acute myocardial infarction; the prevalence of infarction by independent criteria was 0.43. This strategy is based on the sequential application of: (a) clinical criteria; (b) total creatine kinase determinations in two serum samples drawn within 10 to 20 h of the onset of acute symptoms; and (c) creatine kinase B-subunit (S-CK B) determinations after immunoinhibition with antibodies to creatine kinase M-subunit in the reaction medium in all samples found to have increased total creatine kinase activity. Discrimination limits of 150 U/L total creatine kinase for women and 200 U/L for men gave a diagnostic sensitivity of 0.99. Activities less than these limits in samples identified 68% of the 274 non-infarct cases (posterior probability of a negative result of 0.99) within 20 h. Subsequent determination of S-CK B in 292 patients who were positive by the discrimination limits for total creatine kinase verified myocardial infarction in 99% of 207 cases for which S-CK B exceeded the discrimination limit of 12 U/L. The strategy excluded 98% of all non-infarct cases at a posterior probability of 0.99.

Prophylaxis of ventricular tachyarrhythmias with intravenous and oral tocainide in patients with and recovering from acute myocardial infarction.

In a double-blind placebo controlled study, tocainide, 750 mg i.v. during a 15-minute period directly followed by 800 mg orally and later 400 mg t.i.d., was administered to patients wiht acute myocardial infarction (AMI). Treatment was started as soon as possible following onset of symptoms; the follow-up period was 6 months. The patient groups consisted of 56 tocainide and 56 placebo patients. There was no significant effect on the incidence of ventricular fibrillation or symptomatic ventricular tachycardia. The mortality rates were similar and low in both groups. Tocainide suppressed ventricular arrhythmias, including ventricular tachycardia, both in the acute stage of AMI and during convalescence. Tocainide also suppressed exercies-induced ventricular arrhythmias. Side effects were in general mild or moderate.

Serum creatine kinase B subunit activity in diagnosis of acute myocardial infarction.

The value of serum creatine kinase B subunit activity (CK B) in the diagnosis of acute myocardial infarction was studied in 238 consecutive cases. All were admitted to a coronary care unit because of suspected acute myocardial infarction. Serum CK B activity was determined by an immunoinhibition procedure, using a CK M subunit inhibiting antibody (anti-M). For the evaluation of serum CK B, patients were classified into acute myocardial infarction and non-acute myocardial infarction groups. This classification was based on electrocardiographic findings, on quantitative determinations of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total serum creatine kinase (CK) activities, and on qualitative electrophoretic determinations of serum CK and serum lactate dehydrogenase (LD) isoenzymes. The prevalence of acute myocardial infarction in the patient material was 0.47. Serum CK B subunit activity was found to be a highly selective indicator of acute myocardial infarction with a predictive value of a positive test result of 0.97 and a predictive value of a negative test result of 0.99. The serum CK B activity increased above the acute myocardial infarction discrimination limit within 12 hours from onset of symptoms. Two non-acute myocardial infarction patients, who were resuscitated after cardiac arrest, had increased serum CK B values caused by the transient presence of CK isoenzyme BB in serum.

Tocainide kinetics after intravenous and oral administration in healthy subjects and in patients with acute myocardial infarction.

Tocainide is structurally related to lidocaine but may be used orally as well as intravenously. A therapeutic plasma concentration range of 25 to 45 mumole/l has been suggested. Tocainide kinetics were studied in 6 healthy subjects and 16 patients with acute myocardial infarction. There was good accordance in kinetics of healthy subjects and patients. After intravenous administration the mean t1/2 was about 14 hr, volume of distribution about 3.0 l/kg, and corrected renal clearance about 140 ml/min. An average of 35% of the dose was recovered unchanged in urine. After oral administration the absorption rate was rapid relative to the elimination rate, extent of bioavailability was complete, and the apparent volume of distribution was the same as that after intravenous injection. A dose regimen of 750 mg intravenously directly followed by 800 mg orally and subsequently 400 mg 3 times daily resulted in therapeutic plasma levels within 15 min. The plasma levels remained within the therapeutic range throughout a period of observation from 48 to 168 hr.