Raimo Kettunen

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 Most of the existing data are based on the 1970s and are no longer valid for current practice.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 in‐frequent.Elevan percent of patients needed an invasive procedure due to an early or late complication.

Cardiac Sympathetic Denervation in Patients With Coronary Artery Disease Without Previous Myocardial Infarction

Myocardial infarction damages sympathetic nerve fibers coursing through the infarct zone. In this study we investigated whether coronary artery disease without myocardial infarction results in sympathetic denervation. We examined 12 patients without a history of previous myocardial infarction and 19 postinfarction patients. 1-123 metaiodobenzylguanidine (MIBG) and technetium-99m sestamibi (MIBI) single-photon emission tomography were conducted at rest to determine the extent of denervated myocardium and the extent of myocardium with reduced perfusion, respectively. In addition, myocardial perfusion during exercise was assessed with MIBI. A MIBG or MIBI defect was determined as being regional uptake of < or =30% of the maximal myocardial activity. All but 1 patient without previous infarction had MIBG defects. MIBG defects (10.3 +/- 8.5% of left ventricular mass) were significantly larger than MIBI defects at rest (2.4 +/- 3.2%, p <0.001) and during exercise (4.8 +/- 6.1%, p <0.05). In multiregression analysis, the size of an MIBG defect was associated with severity of coronary stenoses (> or =90% of lumen diameter; p <0.05), but not with age, number of significant stenoses (> or =50% of lumen diameter), left main disease, functional class, left ventricular ejection fraction, angina pectoris, maximal ST depression, or mean workload during exercise test. MIBG and MIBI defects were significantly larger in patients with severe coronary stenoses than in patients with moderate stenoses (50% to 89% of lumen diameter) (16.4 +/- 8.9% vs 6.0 +/- 5.2% [p <0.05] and 5.0 +/- 3.1% vs 0.6 +/- 1.3% [p <0.001], respectively). The size of MIBG (16.1 +/- 8.9%) and MIBI defects (7.3 +/- 6.5%) at rest in postinfarction patients did not differ from patients with severe stenoses. Our study demonstrates that cardiac adrenergic tissue is very sensitive to ischemia and that regional cardiac sympathetic denervation can occur in patients with stable coronary artery disease without previous myocardial infarction.

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 training and anabolic steroids on collagen synthesis in dog heart

SummaryThe effects of endurance training and anabolic steroid (Methandienone 1.5 mg · kg−1 p. o. daily) and their combination on regional collagen biosynthesis and concentration in the hearts of male beagle dogs were studied by measuring prolyl 4-hydroxylase (PH) activity and hydroxyproline (HYP) concentration. The PH (P<0.05) and HYP (P<0.05) were both greater in the subendocardinal layer than in the subepicardium (EPI) of the left ventricular wall in controls, whereas opposite gradients (P<0.05) were observed in the right ventricle. Endurance exercise caused an increase of PH activity in EPI of the left ventricular wall (P<0.01). The HYP concentration increased in both layers of the right ventricle in the exercise plus steroid group (P<0.05). The results suggest that transmural differences exist in the rate of collagen synthesis and concentration in canine cardiac ventricles and that endurance exercise may accelerate collagen synthesis in EPI of the left ventricle and the combination of exercise and anabolic steroid causes an increase in collagen concentration in the right ventricular wall.

Usefulness of technetium-99m-MIBI and thallium-201 in tomographic imaging combined with high-dose dipyridamole and handgrip exercise for detecting coronary artery disease

Forty-two patients with known stable coronary artery disease, referred for coronary angiography, were examined with technetium-99m-hexakis-2-methoxy-2-methylpropyl-isonitrile (MIBI) tomography combined with a high-dose dipyridamole infusion (0.7 mg/kg) and handgrip stress. MIBI tomography was unable to show coronary artery disease only in 2 patients, thus yielding a sensitivity figure of 95%. MIBI tomography correctly identified 27 (82%) of 33 stenotic lesions (greater than or equal to 50% diameter stenosis) of the left anterior descending artery, 17 (61%) of 28 of those of the left circumflex artery, and 28 (90%) of 31 of those of the right coronary artery. The overall vessel sensitivity was 78%. The computed lumen diameter stenoses were more advanced in cases detected than in those not detected with MIBI tomography: 87 +/- 14 vs 76 +/- 14% (p less than 0.01). The 50 to 69% stenoses did not show any tendency to produce less positive findings than those with greater than or equal to 70% stenoses. In the subgroup of 21 patients who also presented for thallium scintigraphy, the overall diseased vessel identification rate was 76% for thallium tomography and 83% for MIBI tomography (p = not significant). Minor noncardiac side effects related to the dipyridamole-handgrip test occurred only in 5% of 63 study sessions. A high-dose dipyridamole combined with isometric exercise is a safe stress method, and when used during scintigraphy, MIBI tomography is at least as efficient a tool as thallium tomography in detecting diseased vessel territories in patients in coronary artery disease.

Preoperative diagnosis of coronary artery disease in patients with valvular heart disease using technetium-99m isonitrile tomographic imaging together with high-dose dipyridamole and handgrip exercise

Forty-seven consecutive patients (mean age 61 +/- 8 years) referred for cardiac catheterization due to moderate to severe aortic (n = 30) or mitral (n = 17) valvular heart disease were examined by technetium-99m isonitrile tomography together with a high-dose dipyridamole infusion (0.7 mg/kg) and handgrip stress. Tomography did not identify coronary artery disease (CAD) in 3 of the 21 patients with angiographically proven disease (sensitivity 86%) and suggested false positive results in 5 of the 26 without the disease (specificity 81% and negative predictive accuracy 88%). No patient without angina pectoris and with negative scintigraphy (n = 14) had angiographically significant (greater than or equal to 50% diameter stenosis) CAD. Overall vessel sensitivity was 63%, and specificity was 92%. The frequency of side effects during the dipyridamole-handgrip test was only 7%. No serious complications occurred during stress tests. Thus, technetium-99m isonitrile tomographic imaging, together with high-dose dipyridamole and handgrip exercise, is a useful noninvasive method in excluding significant CAD in patients with valvular heart disease.

The acute dose-related effects of ethanol on right ventricular function in anesthetized dogs

The acute dose-related effects of small to moderate doses of ethanol on right ventricular functioning were studied on 18 anesthetized, artificially ventilated dogs in 39 sessions. Diluted ethanol (from 25-37.5%) was infused during 40 minutes, yielding total doses of 1.0 g/kg (n = 15), and 1.5 g/kg (n = 12) with corresponding venous blood ethanol peak concentrations of 1.38 +/- 0.25 and 2.41 +/- 0.31 mg/ml, respectively. Heart rate increased up to 16% in groups receiving ethanol. In the control group receiving the equivalent volume of saline (n = 12) heart rate decreased 14%. Pulmonary arterial systolic pressure increased from 24 +/- 3 to 27 +/- 3 mmHg and diastolic pressure from 11 +/- 2 to 14 +/- 4 mmHg (p less than 0.05) when the ethanol dose was 1.0 g/kg. The pulmonary arterial resistance increased from 620 +/- 135 to 805 +/- 185 dyn.s.cm-5 (p less than 0.01). The peak dP/dt decreased maximally by 20% with increasing ethanol doses. Stroke volume decreased maximally by 14% but due to the increase in heart rate, cardiac output even increased. The changes in end-diastolic volume and pressure were not significant. Hence, the ethanol increased heart rate and afterload of the right ventricle but depressed the myocardium.

Electromechanical delay in the intact dog heart

A computer method was developed for the determination of electromechanical delay defined as the time between the onset of Q-wave and the onset of the left ventricular systolic pressure rise. It was validated for heart catheterization studies on 56 intact anaesthetized beagle dogs in 86 sessions. The mean basal value of the electromechanical delay was 22 +/- 4 msec. Heart rate, contractility, preload and afterload were changed by atrial pacing and by infusions of calcium chloride, isoproterenol, propranolol, dextran and phenylephrine. Increase of heart rate by pacing from the spontaneous rate of 90 per min to 240 per min prolonged the electromechanical delay from 21 +/- 5 to 33 +/- 14 msec (P less than 0.001). Otherwise the duration of electromechanical delay changed independently of the heart rate. If it changed, the direction of the change followed that of the pre-ejection period. Its proportion of the pre-ejection period varied from 26 to 52%. The electromechanical delay shortened when a positive inotropic effect was noticed or the presystolic fibre length increased.

Cardiac adrenergic denervation in patients with non-Q-wave versus Q-wave myocardial infarction

Abstract.In spite of smaller infarct size and better preserved left ventricular function the long-term prognosis after a non-Q-wave infarction is not better than after a Q-wave infarction. In fact, the risk of sudden cardiac death is higher in patients with a non-Q-wave infarction than in patients with a Q-wave infarction. One possible reason for postinfarction arrhythmias is cardiac adrenergic denervation resulting from myocardial infarction. In this study we compared cardiac adrenergic innervation after non-Q-wave and Q-wave infarctions. Single-photon emission tomography using iodine-123 metaiodobentzylguanidine (MIBG) and technetium-99m sestamibi (MIBI) tracers were conducted in order to compare cardiac adrenergic denervation and myocardial perfusion in 12 patients with a non-Q-wave infarction and 15 patients with a Q-wave infarction. MIBG and MIBI defects were determined as regional uptake ≤30% of maximal myocardial activity. The size of MIBI defects calculated as a percentage of left ventricular mass was significantly smaller in patients with a non-Q-wave infarction than in patients with a Q-wave infarction (4%±3% vs 9%±7%, P<0.05, respectively). According to the maximal serum creatine kinase activity, less myocardium was damaged in patients with a non-Q-wave infarction than in patients with a Q-wave infarction (502±436 IU/l vs 1878± 1265 IU/l, P<0.001). In spite of this, the extent of MIBG defects was similar in patients with a non-Q-wave and patients with a Q-wave infarction (21%±18% vs 23%± 12%, respectively). In addition, the size of MIBG defect correlated with the infarct size (maximal creatine kinase activity) (r=0.52, P<0.05) after a Q-wave infarction but not after a non-Q-wave infarction. In conclusion, despite a smaller infarct size in non-Q-wave infarct patients, the extent of cardiac adrenergic denervation was similar in patients with a non-Q-wave and patients with a Q-wave infarction. In addition, the extent of cardiac adrenergic denervation was related to the infarct size in patients with a Q-wave infarction but not in patients with a non-Q-wave infarction.

Anabolic steroids alter the haemodynamic effects of endurance training on the canine left ventricle

The effects of six week, high-dose anabolic steroid treatment (methandienone, 1.5 mg/kg/day) on the changes in left vetricular function induced in dogs by endurance training were studied by a catheterization technique under anaesthesia. Pacing, isoproterenol and dextran infusions were used as loading tests (respectively). Dogs were randomized into an exercise group (EG,n=7) and an exercise-steroid group (ESG,n=7), the latter receiving anabolic steroids as well as participating in the training program. In a standardized submaximal exercise test, the heart rate of unanaesthetized dogs was lower both in the EG (p<0.001) and in the ESG (p<0.01) after the training period than before it. In the EG the resting systemic vascular resistance (SVR) before haemodynamic interventions was lower (p<0.05) and left ventricular stroke work (SW) was higher (p<0.05) after the training period than before. In the ESG, left ventricular ejection fraction (EF) decreased with training and anabolic steroid treatment (p<0.05). After the training period isoproterenol increased the maximum velocity of the cardiac contractile element significantly more (p<0.05) in the EG than in the ESG. Also SW increased in the EG (29%,p<0.001), but not in the ESG (−11%, NS). Endurance training increased the left ventricular end-diastolic and stroke volumes during isoproternol infusion, but this training effect was attenuated by simultaneous anabolic steroid treatment (p<0.05 between the groups in both case). During the isoproterenol test SVR decreased less in ESG than in EG (p<0.05 between). In volume loading tests, the ESG worked on a higher level of stroke work at a given end-diastolic volume when compared to the EG (p<0.001). This was related to a higher mean aortic ejection pressure and systemic vascular resistance measured in the ESG. In conclusion, the improved cardiac performance and peripheral adaptation after endurance training are partly attenuated by the simultaneous use of anabolic steroids in dogs.