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Biomedical subjects

O J Ohm

Publications and source records attributed to O J Ohm.

At least 19 recordsLinked to original sources

[Sudden cardiac death].

Sudden cardiac death is instant unexpected death that occurs within one hour of an abrupt change in a person's stable clinical state. The mechanism is generally a ventricular tachyarrhythmia. The underlying pathology is usually coronary heart disease. In 1990, 18 patients who survived sudden cardiac death, excluding those with acute myocardial infarction, were evaluated and treated in our institution. 15 patients had coronary heart disease, one had hypertrophic cardiomyopathy, one had dilated cardiomyopathy and one had a replaced aortic valve. Evaluation included heart catheterization and electrophysiological examination. Treatment was specifically tailored to each patient according to etiology, results of all tests and the patient's prognostic factors. Treatment included a permanent pacemaker-cardioverter-defibrillator, antiarrhythmic drug therapy, aortocoronary bypass and betablocker therapy.

Aged

[Intermittent bradyarrhythmia in infants and small children treated with permanent pacemaker].

Four children aged two, two and four months and five years respectively, with intermittent cardiac bradyarrhythmias and otherwise normal hearts are described. The diagnoses were based upon findings by telemetry and 24-hour ECG-recordings. Two patients had sinus node disease, one patient had intermittent complete atrioventricular block, and the fourth had a permanent first degree atrioventricular block and intermittent high grade second degree atrioventricular block. All patients presented serious symptoms with apparent life-threatening events before admission. They were given a permanent cardiac pacemaker. One patient experienced recurrent excessive increase in the myocardial stimulation threshold, leading to further syncopal episodes. All patients are developing adequately with normally functioning pacemakers.

Bradycardia

Efficacy of automatic multimodal device therapy for ventricular tachyarrhythmias as delivered by a new implantable pacing cardioverter-defibrillator. Results of a European multicenter study of 102 implants.

BACKGROUND: Third-generation implantable cardioverter-defibrillators are devices designed to treat ventricular tachycardia (VT) and ventricular fibrillation (VF) by means of overdrive pacing, cardioversion, or defibrillation. So far, the efficacy of tiered therapy has been documented only in small series. Therefore, a European multicenter clinical evaluation study of a new tachyarrhythmia control device, the Medtronic PCD pacer-cardioverter-defibrillator with epicardial patch-lead configuration, was undertaken. METHODS AND RESULTS: We report on 102 patients (mean age, 55 +/- 13 years) from 11 European centers. PCD devices implanted between May 1989 and February 1991 were included. The patients suffered from hemodynamically significant ventricular tachyarrhythmias not suppressed by antiarrhythmic drug therapy and unrelated to acute myocardial infarction; one patient had nonsustained VT and severely depressed left ventricular function. Seventy patients had coronary artery disease with old myocardial infarctions, 23 had cardiomyopathies of various etiologies, and nine patients had no detectable heart disease. Mean ejection fraction was 36 +/- 14% (range, 10-76%). Mean intraoperative defibrillation threshold (51 patients) was 10.6 +/- 5.1 J (range, 2-18 J). The documented follow-up ranged from 1 to 21 months (mean, 9.4 +/- 5.8 months), or 79.9 cumulative patient-years. Perioperative mortality was 3.9%. The actuarial survival rate at 12 months was 91%. One sudden arrhythmic death occurred. Sixty patients (58%) received device therapy. Seventeen patients had therapies only for "VF" episodes, 16 patients only for VT, and 28 patients for VT and "VF" episodes. Based on device memory data, 1,235 spontaneous VT episodes were detected and treated in 43 patients. Twelve hundred four of these VT episodes received painless initial antitachycardia pacing therapy, restoring sinus rhythm in 91%. The 108 ongoing episodes received 209 multiple therapeutic attempts. Eighty-five additional overdrive pacing therapies restored sinus rhythm in 30%. Initial ineffective antitachycardia pacing therapies received 51 cardioversion pulses. The success rate was 61%. Seventy-three additional cardioversion pulses were delivered to backup ineffective pacing therapy as well as ineffective secondary cardioversion pulses. Their success rate was only 40%. Two hundred eighty-six spontaneous episodes were detected in 44 patients as "VF." Overall defibrillation efficacy was 97.6%. CONCLUSIONS: The implanted device nearly eliminates sudden arrhythmic death in patients with documented, potentially fatal ventricular tachyarrhythmias. Automatic tiered therapy is highly effective to restore sinus rhythm, provided that an integrated two-zone tachycardia detection algorithm is used, assigning lower tachycardia rates to overdrive pacing and/or cardioversion and higher tachycardia rates to defibrillation. In general, spontaneous VTs can be terminated by automatic overdrive pacing, and painful or disturbing countershock therapies are not required to terminate the majority of spontaneous VT episodes.

Death, Sudden, Cardiac

The influence of supine relaxation on blood pressure, heart rate and atrial natriuretic peptide in normal subjects.

The effect of recumbent rest on plasma atrial natriuretic peptide (ANP) concentration, mean blood pressure (MBP) and heart rate was studied in 26 normal human volunteers. Plasma ANP concentration, MBP and heart rate were determined after 10 min sitting and after 2, 5, 8, 15 and 30 min of recumbency. During the first 5 min of recumbency there were significant decreases in both MBP (p less than 0.001) and heart rate (p less than 0.001) compared with sitting. There was a small but significant fall in plasma ANP concentration (p = 0.02) after 30 min of recumbency compared with sitting. No further reduction in MBP or heart rate occurred after 5 min supine. The level of MBP following 5 min supine correlated significantly (r = 0.44; p = 0.02) with the plasma ANP concentration 25 min later. Blood pressure and heart rate are highly dependent on posture and relaxation, and plasma ANP concentration in lesser degree. It is necessary to wait for stable baseline values to develop before any comparisons between blood pressure and plasma ANP are done. If it is assumed that a causative relation exists between blood pressure and plasma ANP level, it appears there may be a delay of 20-30 min between a change in blood pressure and the physiological response of plasma ANP level. This observation may have implications for the interpretation of the relation between blood pressure and plasma ANP concentration in healthy individuals.

Adult

Electrophysiologic and clinical effects of flecainide for recurrent paroxysmal supraventricular tachycardia.

The antiarrhythmic effects of flecainide acetate were evaluated in 9 patients with paroxysmal atrioventricular (AV) nodal tachycardia and 17 patients with AV tachycardia. An electrophysiologic study was performed before and after intravenous flecainide acetate, 2 mg/kg body weight, was infused over 15 minutes and was followed by a maintenance infusion of 1.6 mg/kg given over 1 hour to 26 patients and during oral treatment to 15. Treatment with oral flecainide acetate was continued for 14 +/- 5 months. Intravenous flecainide acetate terminated AV nodal tachycardia by blocking the retrograde fast pathway conduction in 7 of 7 patients and AV tachycardia by blocking retrograde conduction in the extranodal pathway in 10 of 10 patients. AV nodal tachycardia and AV tachycardia were noninducible in 8 of 9 patients (90%, p less than 0.001) and 11 of 17 patients (65%, p less than 0.001), respectively. Long-term treatment with oral flecainide acetate suppressed AV nodal tachycardia and AV tachycardia in 8 of 9 patients (90%, p less than 0.001) and 11 of 17 patients (65%, p less than 0.001), respectively. A favorable outcome was associated with block in the accessory pathway after intravenous flecainide acetate and noninducibility during oral treatment. Recurrences preferentially occurred in the younger patients. Flecainide acetate is effective in the acute and long-term management of paroxysmal supraventricular reentry tachycardia by suppressing conduction through the retrograde fast limb of the tachycardia circuit. The clinical effect can be predicted by electrophysiologic testing.

Adolescent

Sudden death caused by heart block in a patient with multiple myeloma and cardiac amyloidosis.

A patient with multiple myeloma and amyloidosis was admitted to hospital following successful cardiopulmonary resuscitation at home. No disturbances in heart rhythm were seen during the first 48 hours of continuous telemetric ECG recording. The patient died from ventricular asystole due to complete atrioventricular block, while he was on a 24-hour Holter monitoring the fifth night in hospital. Patients with known cardiac amyloidosis and syncope should undergo long-term ECG recordings, preferably by telemetry. Repeated registrations may be necessary to discover disturbances in heart rhythm.

Amyloidosis

Combined intoxication with digitoxin and verapamil. The possible inhibition of sensitisation to digitalis-specific antiserum by toxic drug concentrations.

The clinical course in a patient with a combined intoxication with digitoxin (maximal serum level 357 nmol/l) and verapamil is described. The patient received two injections of digitalis-specific antiserum. No adverse reactions to the therapy was seen, and the antiserum markedly shortened the plasma half-life of digitoxin. In vitro studies indicate that digitoxin in concentrations seen during the intoxication may have an immunosuppressive effect, thereby reducing the risk of sensitisation to the antiserum.

Aged

A time-related study by Doppler and M-mode echocardiography of hemodynamics, heart size, and AV valvular function during activity-sensing rate-responsive ventricular pacing.

Noninvasive Doppler and M-mode echocardiography were used to: measure stroke volume (SV), left atrial (LA) size, left ventricular end-diastolic (EDD), end-systolic dimensions (ESD), left ventricular fractional shortening (FS), and for determination of mitral and tricuspid insufficiency (MI and TI) before starting and after 1, 3, and 6 months of rate-responsive ventricular pacing (RRP). The study group consisted of 13 patients (mean age, 75 years) who could be expected to benefit from an increase in cardiac output mediated by an increment of heart rate during exercise. In VVI + activity mode (RRP), the pacemaker was programmed to a basic heart rate of 60 and a maximum heart rate of 125 bpm. The SV at rest was 71 +/- 5 before RRP, and fell to 57 +/- 4 after 3 months (p less than 0.05) and to 53 +/- 4 ml/beat after 6 months of RRP (p less than .01). The LA size and ESD were unchanged during follow-up. The EDD decreased from 6.2 +/- 0.3 to 5.4 +/- 0.2 (p less than 0.002) during the first 6 months of RRP. The FS was reduced from 33 +/- 4 to 27 +/- 3% (p less than 0.02) during the first 6 months of RRP. Four of 6 patients treated previously with a VVI pacemaker (mean duration, 9 years) had MI + TI, and 3 of the 7 patients not paced previously had MI before RRP. In the last group, 1 new patient developed MI, 1 new patient developed MI + TI, and 2 patients who had MI also developed TI within 6 months of pacing. Thus, of 13 patients, 9 (69%) had either MI or MI + TI.

Aged

Assessment of the work capacity and relationship between rate response and exercise tolerance associated with activity-sensing rate-responsive ventricular pacing.

The relationship between rate response and exercise tolerance was studied by measuring the symptom-limited maximum treadmill time (MTT)both during fixed rate VVI pacing and during VVI + activity mode pacing (RRP) in 15 patients (mean age, 73 years) who had received rate-responsive ventricular pacemakers. Their indications were atrioventricular block, sino-atrial block, and atrial fibrillation with slow ventricular response. Basic rate was programmed to 60 ppm in both pacing modes; rate response and activity threshold were programmed to 5 and medium, respectively. The order in which the two pacing modes were tested was randomly determined. The MTT was, on average, 29% longer in RRP than in VVI mode with a mean of 12 minutes in VVI and 14.8 minutes in RRP (p less than 0.001). For the subgroup of eight patients with paced-only rhythm the average increase in MTT was 38% with a mean of 9.5 minutes in VVI and 12.8 minutes in RRP (p less than 0.01). Seven patients who showed episodes of spontaneous rhythm, increased their average MTT by 17% (mean in VVI, 14.9 minutes; in RRP, 17.1 minutes; p less than 0.02). During RRP, a significant positive correlation existed between MTT and the increase in heart rate (N = 15; r = 0.83; p less than 0.001). In 12 patients with paced-only rhythm, the pacing rate remained at the programmed basic rate when the patients were lying, sitting, and standing and increased to 86 +/- 4 ppm during casual walking, and to 101 +/- 4 ppm during jumping up and down with the pacemaker programmed to the above-mentioned parameters. The maximum pacing rate during jumping corresponded with the maximum pacing rates measured from Holter recordings during normal daily activities.

Aged

Noninvasive assessment by Doppler and M-mode echocardiography of hemodynamic responses to temporary pacing and to ventriculoatrial conduction.

A new, dual-chamber temporary pacing lead was introduced via the subclavian vein in 20 patients who needed a temporary pacemaker. Stroke volume (SV) was measured continuously by combining M-mode and noninvasive Doppler echocardiography during spontaneous rhythm (SR), AV sequential pacing at a positive AV interval (DP), ventricular pacing (VP) and AV sequential pacing at a negative AV interval (VA pacing). The valvular functions were determined by Doppler echocardiography. Left ventricular dimensions and function, and left atrial size were measured by M-mode echocardiography. In the nine patients with no valvular heart disease and with no ventriculoatrial (VA) conduction (group I) the CO increased 83 +/- 11% during DP and 42 +/- 9% during VP as compared to during SR when the heart rate (HR) was increased from 34 +/- 3 to 72 +/- 1 beats/min. The CO was 29 +/- 3% higher during DP than that during VP. In the seven patients with valvular heart disease and with no VA conduction (group II), the increment in CO compared to that during SR was 53 +/- 12% during DP and 31 +/- 11% during VP; the CO was 17 +/- 4% higher during DP than that during VP. In the four patients with spontaneous VA conduction (group III), the CO during DP was 35 +/- 10% greater than that during VP, which did not result in an increase in the CO compared to that during SR in spite of an increase in HR from 52 +/- 8 to 74 +/- 2 beats/min. The study demonstrated that DP is the preferred temporary pacing mode and also that VA conduction during VP resulted in a mean decrease of 20% in CO compared to that during VP without VA conduction. The hemodynamic benefit from DP compared to SR seems to decrease when the left ventricular end-diastolic dimension increases. Furthermore, patients with large left ventricular end-systolic dimensions seem to have a lower increase in stroke index during DP as compared to that during VP than patients with smaller end-systolic dimensions.

Aged

Ventricular tachyarrhythmia initiation in a canine model of recent myocardial infarction. Comparison of unipolar cathodal, anodal and bipolar stimulation.

Ventricular tachyarrhythmia initiation was compared using unipolar cathodal, anodal and bipolar programmed stimulation at 21 sites in 5 normal adult mongrel dogs and 67 noninfarct sites in 16 dogs 3-5 days after experimental myocardial infarction. For this purpose, the minimum number of extrastimuli required for tachyarrhythmia initiation was determined in each pacing mode using twice cathodal threshold current for the drive beats and all extrastimuli except the last. The current and pacing mode were varied for the last extrastimulus (S2, S3 or S4). In the 5 normal dogs, ventricular fibrillation was reproducibly inducible from only 1/21 sites, and only in the cathodal mode. In 15/16 (94%) of the myocardial infarction dogs, a sustained ventricular tachycardia or ventricular fibrillation could be reproducibly initiated with either one (4 dogs), two (5 dogs) or three extrastimuli (6 dogs). Diastolic excitability thresholds were 0.08 +/- 0.03, 0.30 +/- 0.17, and 0.09 +/- 0.04 mA (median +/- SD) for unipolar cathodal, anodal and bipolar pacing, respectively (p less than 0.001 for anodal vs. cathodal and bipolar). The median absolute current required for ventricular tachyarrhythmia initiation was also highest with anodal pacing (0.72 +/- 0.77 mA), versus both the cathodal and anodal modes (0.18 +/- 0.28 and 0.20 +/- 0.28 mA, respectively, each p less than 0.001) but was comparable in all three modes relative to the threshold current (2.0, 2.4 and 2.6 mA for cathodal, anodal and bipolar pacing, respectively) required for initiation. Overall, ventricular tachyarrhythmia initiation was concordant in all three modes at 58/67 (87%) sites and discordant at only 9/67 (13%) sites (p less than 0.001). Moreover, there was no difference in either the pattern of arrhythmia initiated in each of the pacing modes with respect to ventricular tachycardia versus ventricular fibrillation, or in the median current required to initiate ventricular tachycardia (0.30 +/- 0.36 mA) versus ventricular fibrillation (0.31 +/- 0.44 mA; p greater than 0.1). Thus, ventricular tachyarrhythmia initiation was comparable in all three pacing modes with respect to overall success rate, number of ventricular extrastimuli required and the pattern of ventricular tachyarrhythmia initiated. Bipolar pacing with similar size anodal and cathodal electrodes appear to be appropriate for electrophysiologic ventricular tachyarrhythmia studies and are not likely to induce spurious arrhythmias resulting from stimulation at the anodal pole.

Animals

Hypertrophic cardiomyopathy in three generations of a large Norwegian family. A clinical, echocardiographic, and genetic study.

Hypertrophic cardiomyopathy is a heart muscle disease with an obscure aetiology. Data from four generations of a large family (71 members) are presented. The occurrence of hypertrophic cardiomyopathy among members of the two oldest generations was compatible with a pattern of autosomal dominant inheritance. Seven out of 14 siblings in the second generation had definite signs of or were clinically suspected of having hypertrophic cardiomyopathy. The severity and distribution of left ventricular hypertrophy varied, but three (21%) brothers in generation II showed the classic picture of left ventricular outflow obstruction. Four siblings (29%) died suddenly aged 11, 22, 38, and 40 years. A high incidence of the disease would have been expected in the two younger generations (41 members, aged 1-31 years), but only two, a 16 year old boy and a 17 year old girl had signs of asymmetric septal hypertrophy. Current diagnostic procedures, including M mode and cross sectional echocardiography, are not sufficiently sensitive to identify young family members who may have preclinical hypertrophic cardiomyopathy. No evidence for close genetic linkage between a postulated locus for hypertrophic cardiomyopathy and the major histocompatibility complex (antigens HLA-A, HLA-B, and HLA-DR) was found.

Adolescent

Splanchnic extraction of oestrone and oestradiol and production of oestrone sulphate in man.

The plasma concentrations of oestrone (Oe1), oestradiol (Oe2) and oestrone sulphate (Oe1S) were measured in the femoral artery (FA), femoral vein (FV) and hepatic vein (HV) in seven men and three postmenopausal women undergoing catheterization for the evaluation of cardiac arrhythmias. None of the persons had congestive heart failure; conventional liver function tests were normal, and they were without any medication. The plasma concentration (mean +/- SD) for Oe1 was 34.6 +/- 19.5 pM in HV, 134 +/- 71.6 pM in FV and 93.4 +/- 48.5 pM in FA. The plasma concentration of Oe2 was 29.9 +/- 19.7 pM in HV, 80.3 +/- 42.7 pM in FV and 55.2 +/- 28.1 pM in FA. The results support the concept of peripheral formation of Oe1 and Oe2 and hepatic removal. The plasma concentration of Oe1S was 980 +/- 469 pM in HV, 945 +/- 463 pM in FV and 937 +/- 461 pM in FA. The small difference in plasma level of Oe1S between FA and FV was insignificant. In all persons the plasma level of Oe1S was higher in HV than in FA and FV (2P less than 0.01) indicating a net formation of Oe1S in the splanchnic area.

Adult

Importance of the pacing mode in the initiation of ventricular tachyarrhythmia in a canine model of chronic myocardial infarction.

The use of unipolar anodal or bipolar pacing, as compared with unipolar cathodal pacing, purportedly increases the likelihood of inducing inadvertent ventricular fibrillation in susceptible patients. In this study, the ability to initiate sustained ventricular tachycardia or fibrillation with unipolar cathodal, unipolar anodal and bipolar pacing modes was compared using programmed ventricular stimulation at 82 subendocardial periinfarction sites in 11 dogs with chronic myocardial infarction. The late diastolic excitability threshold was significantly higher and the ventricular refractory period was significantly shorter (p less than 0.001) with anodal pacing (mean 0.62 mA, 156 ms, respectively) than with pacing in either the cathodal (0.12 mA, 174 ms) or the bipolar (0.13 mA, 173 ms) mode. At a current intensity twice that of the excitability threshold, the introduction of one or two extrastimuli induced ventricular tachycardia and ventricular fibrillation comparably among the three pacing modes. However, when three extrastimuli were used, ventricular fibrillation was induced with anodal pacing twice as frequently (50 [61%] of 82 sites) as with either of the other two pacing modes (each 23 [28%] of 82 sites, p less than 0.001), whereas the induction of ventricular tachycardia remained comparable with anodal pacing (15 [18%] of 82 sites) and cathodal and bipolar pacing (each 14 [17%] of 82 sites). Furthermore, a similarly high incidence of inducibility of ventricular fibrillation was observed with both cathodal pacing (56 [68%] of 82 sites) and bipolar pacing (40 [49%] of 82 sites) when an increased current equal to twice the anodal excitability threshold (1.23 mA) was used.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

A time-related study of the hemodynamic benefit of atrioventricular synchronous pacing evaluated by Doppler echocardiography.

We have used Doppler echocardiography to estimate the stroke volume (SV) in a study of 13 patients equipped with DDD pacemakers. SV was measured both during DDD and VVI pacing after observation times of 1,3,6, and 12 months of DDD pacing. SV was also measured at seven atrioventricular (AV) intervals (75-250 ms) in the search for optimal AV intervals. Mitral flow velocity was investigated to see if DDD pacing resulted in synchronous atrial contraction, and if mitral insufficiency existed at any of the pacing modes. Compared with the VVI mode, DDD pacing resulted in a mean increase in SV of 21 +/- 2% for the four observation periods. Two patients with severe left ventricular failure had no significant increase in SV during DDD vs VVI pacing. In each patient, an optimal AV interval ranging between 100-250 ms for the SV was found. Velocity profiles of mitral flow showed synchronous atrial contraction during DDD pacing, but not during VVI pacing. Mitral insufficiency was not seen in any pacing mode. DDD pacing resulted in a reduction in SV during the first 6 months, and was constant thereafter. Doppler echocardiography can be used repeatedly to evaluate the hemodynamic response of DDD pacing vs VVI pacing, and to find which AV interval gives the highest SV in the individual patient. Our study further shows that the hemodynamic benefit of DDD pacing is present after short-term as well as after long-term DDD pacing.

Adult

Sick sinus syndrome treated with permanent pacemaker in 109 patients. A follow-up study.

During the last decade implantation of permanent pacemakers has become the treatment of choice for patients suffering from the sick sinus syndrome (SSS). We have followed up 112 SSS patients treated with permanent pacemakers in Haukeland Hospital in the period 1966--76. The pacemakers were later removed from three of the patients. In the remaining 109 patients the SSS was characterized by tachy-bradyarrhythmias (TBA) in 44 and bradyarrhythmias (BA) in 65. Before implantation, 68 patients had syncopes and 27 severe dizziness. After implantation, symptomatic improvement was apparent in 104 patients; only three still had syncopes. During the follow-up period (mean 34.4 months), 29 patients died (yearly mortality 9.3%). There was no significant difference in total mortality between patients with TBA and with BA. Concomitant disturbances in atrioventricular (AV) conduction occurred in 35.8% of the patients. Among 79 of 80 patients still alive, five had developed total AV block, 19 had stable atrial fibrillation, 12 of these were possibly pacemaker-independent (ventricular rate greater than 60/min). Systemic embolization was observed in 16 patients, more frequently in the TBA (12/44) than in the BA group (4/65) (p less than 0.001). It is concluded that permanent pacemakers have an excellent symptomatic effect in patients with SSS. The prognosis is mainly determined by the presence or absence of coronary heart disease and/or heart failure.

Adolescent