Complications related to permanent pacemaker therapy.

This study evaluates complications related to permanent endocardial pacing in the era of modern pacemaker therapy. There is only limited information available about the complications related to modern cardiac pacing. Most of the existing data are based on the 1970s and are no longer valid for current practice. The recent reports on pacemaker complications are focused on some specific complication or are restricted to early complications. Thus, there are no reports available providing a comprehensive view of complications related to modern cardiac pacing. Four hundred forty-six patients, who received permanent endocardial pacemakers between January 1990 and December 1995 at Kuopio University Hospital, were reviewed retrospectively using patient records. Attention was paid to the occurrence of any complication during the implantation or follow-up. An early complication was detected in 6.7%, and 4.9% of patients were treated invasively due to the early complication. Late complication developed in 7.2% and reoperation was required in 6.3% of the patients. Complications related to the implantation procedure occurred in 3.1%. Inadequate capture or sensing was observed in 7.4% of the patients. Pacemaker infection was detected in 1.8% and erosion in 0.9% of the patients. An AV block developed in 3.6% (1.6%/year) patients who received an AAI(R)-pacemaker due to sick sinus syndrome. There was no mortality attributable to pacemaker therapy. A great majority (68%) of the complications occurred within the first 3 months after the implantation. Complications associated to modern permanent endocardial pacemaker therapy are not infrequent. Eleven percent of patients needed an invasive procedure due to an early or late complication.

Prevalence and natural course of ectopic atrial tachycardia.

AIMS: The purpose of this study was to calculate the prevalence of ectopic atrial tachycardia in a population of young asymptomatic males and to assess its natural course both in asymptomatic subjects and in symptomatic hospital patients. METHODS AND RESULTS: 12-lead electrocardiograms (ECG) of 3554 consecutive males applying for a pilot's licence were analysed. ECGs of symptomatic arrhythmia patients at two university hospitals were also analysed. A repeat ECG was taken in cases of ectopic atrial tachycardia to assess the natural course of this arrhythmia. Twelve out of 3554 asymptomatic subjects (prevalence 0.34%) and 17 out of 3700 symptomatic arrhythmia patients (prevalence 0.46%) had ECG evidence of ectopic atrial tachycardia. A repeat ECG was obtained after a mean follow-up of 8+/-3 years in asymptomatic subjects and 7+/-3 years in symptomatic patients. After the follow-up, seven (26%) out of 27 patients were still in a similar ectopic atrial rhythm, 10 (37%) showed a change in P wave morphology and 10 (37%) were in sinus rhythm. Heart rate was significantly slower (mean rate 81+/-19 vs 109+/-17 beats. min-1) in the repeat ECGs. CONCLUSION: Asymptomatic ectopic atrial tachycardia is not an uncommon finding in a population of young males. The majority of patients show slowing of heart rate in the course of time, either with restoration of sinus rhythm or with a change in P wave morphology, suggesting that the ectopic foci undergo gradual degeneration with time.

The acute dose-dependent effects of ethanol on canine myocardial perfusion.

The acute effects of ethanol (1.0 g/kg and 1.5 g/kg, n = 4 and n = 5, yielding blood concentrations of 1.3 +/- 0.2 mg/ml and 2.4 +/- 0.3 mg/ml) on myocardial perfusion were studied in anesthetized, thoracotomized, artificially ventilated dogs by using a radioactive microsphere technique. The control group (n = 5) received saline. The smaller dose of ethanol decreased perfusion in the left ventricular myocardium from 0.737 +/- 0.122 to 0.555 +/- 0.122 ml/g/min (NS), whereas the greater dose nonsignificantly increased it, from 0.744 +/- 0.115 to 0.819 +/- 0.119 ml/g/min (p < 0.01 between the groups). These changes were most evident in subendocardial layers (p < 0.01 both within the groups and between the groups). The greater dose of ethanol increased systemic vascular resistance (p < 0.01 when compared to the control group). The changes in right ventricular myocardium were insignificant. The acute effect of ethanol on coronary blood flow is dose-dependent with small to moderate doses reducing demand for left ventricular flow but with increasing doses evoking not only an increase in demand for flow but also an increase in flow.

Plasma N-terminal atrial natriuretic peptide in acute myocardial infarction.

Plasma atrial natriuretic peptide (ANP) and the N-terminal (NT) fragment of the 126-amino acid prohormone of ANP (proANP; NT-proANP) were correlated with clinical findings in 41 patients with acute myocardial infarction and in 19 patients with angina pectoris. On admission to the hospital, the 39 patients with nonfatal infarction who subsequently had overt heart failure (n = 8) had plasma NT-proANP (2374 +/- 1038 pmol/L) and ANP (54 +/- 43 pmol/L) concentrations that were higher (p < 0.01) than those in the patients who remained without or who presented with minor signs of failure. In contrast to the relatively stable NT-proANP levels, ANP decreased markedly during the first 24 hours in the patients who had any signs of failure. Hence the plasma levels of NT-proANP and ANP did not go hand in hand in acute myocardial infarction, and NT-proANP appeared to be a better marker of cardiac dysfunction than ANP.

Effects of early administration of enalapril on radionuclide left ventricular ejection fraction and plasma N-terminal atrial natriuretic peptide after acute myocardial infarction.

The effects of enalapril therapy on radionuclide ejection fraction and plasma N-terminal atrial natriuretic peptide were investigated in a randomized, double-blind, placebo-controlled study of 52 patients with acute myocardial infarction. The medication was begun intravenously within 24 hours of the onset of symptoms. At discharge and the end point of 6 months, the radiographic size of the heart was significantly smaller in patients receiving (n = 28) than in those not receiving (n = 24) enalapril therapy (p < 0.03 vs < 0.01). However, left ventricular ejection fraction decreased simultaneously from 50 +/- 10% to 47 +/- 11% in patients treated with enalapril, whereas it increased from 48 +/- 13% to 50 +/- 14% in control patients (p < 0.05 for the difference of the changes). The decrease in ejection fraction was most marked in the infarct-related region of the left ventricle (p < 0.01). During the in-hospital period, plasma N-terminal atrial natriuretic peptide was decreased in patients treated with enalapril, whereas it was increased in those treated with placebo with complicated acute myocardial infarction (p < 0.05). During the following 6 months, the differences remained insignificant. Early administration of enalapril significantly attenuated heart enlargement after myocardial infarction and probably improved hemodynamics during the acute phase of complicated infarction. The decrease in ejection fraction during recovery indicates an impairment of systolic function. The decrease in infarct-related regional ejection fraction suggests that the impairment may be due to poor healing of the infarction scar.