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Biomedical subjects

L Toivonen

Publications and source records attributed to L Toivonen.

At least 109 records · Page 6Linked to original sources
PubMed1991

Coronary collateral circulation.

The occurrence and influence of coronary collateral circulation and obstruction of the supplying coronary arteries on left ventricular contractility, prevalence of myocardial infarction, and bicycle exercise ergometer test were studied in a random sample of 286 patients with angiographically documented coronary artery disease. Collaterals appeared increasingly in all three main coronary arteries with grade of obstruction. The highest prevalence of collaterals occurred in stenosis of the right coronary artery (60%), followed by the left descending artery (45%); they occurred least in the left circumflex artery (21%) (p less than 0.001). The frequency of intra-arterial collateral circulation was 42%, 11%, and 12%, respectively (p less than 0.001). With total occlusion of the left anterior descending coronary artery, 22% of the patients had normokinetic anterior and apical left ventricular wall when collaterals were present. More often, the inferior wall showed normal contraction with total occlusion of the right coronary artery and collaterals [52%, p less than 0.001 compared with left anterior descending artery (LAD)]. The prevalence of inferior myocardial infarction was 39%, with collateral circulation to the totally occluded right coronary artery. The respective prevalence of anterior infarction and total occlusion in the left coronary artery was 58% (p less than 0.02). The presence or absence of collaterals had no obvious influence on ST-segment response during bicycle ergometer test. In triple-vessel disease, peak work capacity was better when collaterals to LAD were not jeopardized (427 kpm) than when jeopardized (321 kpm) (p less than 0.02).

Analysis of Variance↗
PubMed1991

The influence of elevated 50 Hz electric and magnetic fields on implanted cardiac pacemakers: the role of the lead configuration and programming of the sensitivity.

The influence of the electromagnetic interference (EMI) on performance of 15 implanted cardiac pacemakers (12 generator models) was tested during exposure at a high voltage substation. All patients had an adequate spontaneous heart rate during the study. Tests were performed in the ventricular inhibited mode with unipolar sensing in all pacemakers and repeated with bipolar sensing in four pacemakers. The sensitivity was set to a regular, functionally proper level and then to the highest available level. Exposure was done to moderate (1.2-1.7 kV/m) and strong (7.0-8.0 kV/m) electric fields, which correspond to the immediate vicinity of 110 and 400 kV power lines, respectively. In moderate electric fields the output was inhibited in one pacemaker at regular sensitivity (1.7-3.0 mV) and in five pacemakers at the highest sensitivity (0.5-1.25 mV). In strong electric fields the output was inhibited in five pacemakers at regular sensitivity and several pacemakers converted to noise reversion mode at the highest sensitivity. In bipolar mode only one of four pacemakers at high sensitivity (0.5-1.0 mV) was inhibited in the strongest electric field, whereas all four did so in the unipolar mode. One pacemaker with unipolar sensitivity at 0.5 mV was interfered by 63 microT magnetic field. The results confirm that the programmed sensitivity level and the lead configuration markedly influence pacemakers' vulnerability to EMI. Bipolar sensing mode is rather safe in the presence of EMI, which is encountered in public environments. The programmable features of today's pacemakers permit individualized, less stringent safety measures to avoid electromagnetic hazards.

Adult↗
PubMed1991

A prospective comparison of class IA, B, and C antiarrhythmic agents in combination with amiodarone in patients with inducible, sustained ventricular tachycardia.

BACKGROUND: Clinical experience suggests that combinations of antiarrhythmic agents provide more effective control of ventricular tachyarrhythmias than does therapy with single agents. METHODS AND RESULTS: Antiarrhythmic and electrophysiological effects of three class I antiarrhythmic agents, one from each subclass A, B, and C, were assessed in single use and in combination with amiodarone in patients with inducible, sustained ventricular tachycardia that was not suppressed by monotherapy with these agents. Thirty-one patients underwent an electrophysiology test on four occasions: at baseline; after 2-4 days of treatment with quinidine, mexiletine, or encainide; after 2 weeks of treatment with 1,200 mg/day amiodarone; and last, after 2-4 days of treatment with both amiodarone and the previously tested class I agent. The combination of a class I agent and amiodarone prevented the induction of sustained ventricular tachycardia in only one of 31 (3%) patients. Ventricular tachycardia became hemodynamically stable in 11 of 31 (34%) patients because of a marked prolongation in the tachycardia cycle length. It increased from 323 +/- 39 to 423 +/- 84 msec (n = 11, p less than 0.01) by adding encainide to amiodarone therapy, and it showed a tendency to lengthen when quinidine was added to amiodarone (from 373 +/- 77 to 425 +/- 58 msec; n = 10, NS). Each class I agent increased amiodarone-induced depression in myocardial conduction, but the extent of the additional depression seemed to differ among the three subclasses. Ventricular refractoriness was increased by all class I agents when used in combination with amiodarone, although not by mexiletine or encainide when used alone. CONCLUSIONS: Class I antiarrhythmic agents slow ventricular conduction and increase ventricular refractoriness when used in combination with amiodarone. When amiodarone and class I drugs by themselves do not suppress the induction of ventricular tachycardia, the combination of amiodarone and a class I agent seldom results in noninducibility; however, it often lengthens the ventricular tachycardia cycle length and may render the ventricular tachycardia hemodynamically stable.

Amiodarone↗
PubMed1990

Hemodynamic effects of pindolol and atenolol at rest and during isometric exercise: a noninvasive study with healthy volunteers.

Hemodynamic effects of intravenous and oral pindolol and atenolol were assessed in ten healthy volunteers by left ventricular echocardiography and systolic time intervals. Measurements were made at rest and during hand-grip-induced isometric exercise. Drug doses were pindolol 0.015 mg/kg intravenously and 10 mg/day orally, atenolol 0.1 mg/kg intravenously, and 50 mg/day orally. Heart rate at rest was reduced by both drugs. The reduction caused by atenolol during oral treatment was significantly greater (p less than 0.01). Intravenously only pindolol reduced mean arterial pressure. During oral treatment atenolol reduced the mean arterial pressure nonsignificantly. Both drugs lowered heart rate during isometric exercise, atenolol being significantly more effective. During oral treatment atenolol blunted the heart-rate reaction to exercise. Mean arterial pressure during isometric exercise rose slightly with both drugs after intravenous administration. During oral treatment only atenolol reduced the mean arterial pressure significantly. Intravenous atenolol reduced cardiac contractility at rest, indicated by significant decreases in fractional shortening, ejection fraction, and the mean velocity of circumferential fiber shortening. In contrast, intravenous pindolol and oral therapy with either drug did not change contractility. Intravenous atenolol raised total peripheral resistance. The preejection period/left ventricular ejection time ratio decreased with intravenous pindolol, while atenolol increased it. In conclusion, atenolol had more negative inotropic and chronotropic effects, especially after acute intravenous administration. Only atenolol reduced cardiac output and increased peripheral resistance. After repeated oral administration, these effects were less apparent.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1990

Determinants of the ventricular rate during atrial fibrillation.

Determinants of the ventricular cycle length during atrial fibrillation were examined in 52 patients. Thirty-three patients had structural heart disease and none had an accessory atrioventricular (AV) connection. The AV node effective and functional refractory periods, the shortest atrial pacing cycle length associated with 1:1 conduction, the AV node conduction time and indexes of concealed conduction in the AV node were measured in the baseline state (36 patients) and after modification of sympathetic tone by infusion of isoproterenol or propranolol (8 patients each). Atrial fibrillation was then induced with rapid atrial pacing, and the mean, shortest and longest ventricular cycle lengths were measured. Variables that correlated most strongly with the mean RR interval during atrial fibrillation were the AV node effective refractory period (r = 0.93; p less than 0.001), AV node functional refractory period (r = 0.87; p less than 0.001) and shortest atrial pacing cycle length associated with 1:1 conduction (r = 0.91; p less than 0.001). The AH interval during sinus rhythm (r = 0.74; p less than 0.001) and during atrial pacing at the shortest cycle length with 1:1 conduction (r = 0.52; p less than 0.001) had weaker correlations. Measures of concealed conduction did not improve the prediction of the mean or longest ventricular cycle length during atrial fibrillation. In conclusion, the refractory periods and conductivity of the AV node are the best indicators of the potential of the node to transmit atrial impulses to the ventricles during atrial fibrillation. The degree of concealed conduction in the AV node is a less important determinant of the mean ventricular rate during atrial fibrillation.

Atrial Fibrillation↗
PubMed1990

Haemodynamic effects of bopindolol and atenolol in coronary artery disease. A noninvasive study.

Bopindolol, a new non-selective betablocker, and atenolol, a conventional betablocker, were studied in parallel groups of eight normotensive patients with NYHA II-III angina pectoris. Non-invasive haemodynamic measurements were made using echocardiography and systolic time intervals. Drug doses were 1 mg bopindolol and 100 mg atenolol once daily; measurements were made immediately and at one and six weeks intervals. Both drugs reduced heart rate, atenolol from 62 to 47 beats/minute (24%, P less than 0.01) and bopindolol from 64 to 56 beats/minute (13%, P less than 0.05) at 24 hours. Only atenolol reduced mean blood pressure. Rate pressure product was persistently reduced by atenolol (30% at 24 hours), while with bopindolol this effect lessened with time. Opposite trends in left ventricular enddiastolic and endsystolic diameters were observed; with atenolol tending to increase and bopindolol to lower them. Atenolol had no influence on cardiac contractility, while bopindolol increased it, which was shown by enhancements in the fractional shortening, ejection fraction and maximum velocity of fibre shortening. Neither drug changed peripheral vascular resistance or systolic time intervals. Two patients on bopindolol left the study because of worsening symptoms of coronary artery disease, and two on atenolol owing to side effects, bradycardia and syncope in one and diarrhea in the other. In conclusion, bopindolol showed less beta-blocking effect than atenolol and it had a positive inotropic effect. Its benefit in treating coronary artery disease remains to be proved.

Atenolol↗
PubMed1988

Haemodynamic effects of atenolol and bopindolol at rest and during isometric exercise. A non-invasive study in healthy volunteers.

Circulatory effects of bopindolol, a new nonselective beta blocking agent with intrinsic sympathomimetic activity and atenolol were compared. After baseline and first dose measurements atenolol 25 mg twice daily and bopindolol 1 mg daily were given to 10 healthy young subjects. Haemodynamic measurements were made noninvasively using echocardiography and systolic time intervals. Clinical and circulatory indices were measured at baseline, after initial dose and after one week of regular treatment at rest and at isometric handgrip exercise (IE) (HG). Atenol reduced the heart rate from 62 bpm to 49 and blunted totally the HR increase during IE (p less than 0.01). Bopindolol caused a 10% fall in heart rate (NS) at rest and a 15% fall (p less than 0.05) during IE. BP fell by 6% after atenol administration and 4% after bopindolol (NS) at rest and similarly during IE. In contrast to bopindolol, atenolol caused small increases initially in left ventricular end-diastolic dimension (LVEDD) and left ventricular end-systolic dimension (LVESD). A 10% increase in FS was seen at rest after bopindolol administration (NS). With the fall in heart rate the estimated cardiac output (CO) also fell from 3.66 to 3.151/min (P less than 0.05) after atenolol but rose from 3.87 to 3.93 after bopindolol (NS) during chronic treatment. Consecutively the total peripheral resistance (TPR) was increased to some extent by atenolol, whereas bopindolol reduced it at rest and during IE. A similar response was also found in systolic time intervals PEP/LVET which were reduced during bopindolol administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1987

Spontaneous variability in the frequency of ventricular premature complexes over prolonged intervals and implications for antiarrhythmic treatment.

Spontaneous variability in the frequency of premature ventricular complexes (VPCs) during ambulatory electrocardiography was examined over short (2- to 14-day) and long (6- to 12-month) periods in 20 patients. The coefficient of variation of the mean daily VPC frequency was significantly lower in the short-term periods than the long-term periods. The 95% confidence limit for spontaneous variation in mean daily arrhythmia frequencies was estimated with a linear regression method comparing two 1-day electrocardiographic recordings. The relative reduction in VPCs reaching the confidence limit calculated from the short-term periods was 69% at the beginning and 73% at the end of the 6- to 12-month follow-up. Corresponding values for repetitive VPCs were 78% and 77%. In comparing 2 recordings separated by the long interval, the reductions required were 98 to 100% for all VPCs, and even a 100% reduction was not significant for repetitive VPCs. The number of VPCs fell spontaneously below the initial confidence limit in 8 of 20 patients in later assessments. Thus, apparently positive individual responses are achieved in long-term treatment studies if stringent efficacy criteria are not followed. The variability between recordings over short periods remains fairly constant when reassessed after a long interval, even if the frequency of arrhythmias changes over the long interval. This permits application of conventional percentage limits in evaluation of therapeutic effects if the natural extent of the arrhythmias is periodically reassessed.

Anti-Arrhythmia Agents↗
PubMed1987

Hemodynamic effects of pirmenol and lidocaine: a placebo-controlled, double-blind, comparative study.

The acute hemodynamic effects of pirmenol and lidocaine were studied in a double-blind, placebo-controlled investigation. Thirty patients undergoing catheterization received one of the following: pirmenol as a 50-mg intravenous bolus injection followed by a 2.5 mg/min infusion, lidocaine as a 75-mg intravenous bolus injection followed by a 3 mg/min infusion or placebo administered in a similar fashion. Mean plasma pirmenol concentrations during steady infusion were 2.3 to 2.4 mg/liter, and mean plasma lidocaine concentrations were 16 to 24 mumol/liter. Pirmenol increased heart rate from baseline by 10 beats/min (p less than 0.001) and mean arterial pressure by 5 mm Hg (p less than 0.001), with similar increases in systemic (p less than 0.05) and pulmonary vascular resistance (p less than 0.01). Lidocaine induced a comparable increase in mean arterial pressure (6 mm Hg, p less than 0.001), but unlike pirmenol, it increased left ventricular and diastolic pressure by 2.8 mm Hg (p less than 0.05). Indexes of left ventricular work were not affected by either drug. Echocardiographic ejection fraction was reduced more by pirmenol (-0.05, p less than 0.0001) than by lidocaine (-0.03, p less than 0.05), a difference that may be related to the changes in heart rate. Side effects were not observed in any patient. The myocardial depressant effect of pirmenol is relatively slight and comparable to that of lidocaine.

Adult↗