Lennart Bergfeldt

The Effect of Ventricular Activation Sequence on Cardiac Performance During Pacing

The aim of this study was to evaluate the importance of a normal ventricular activation pattern for cardiac performance. In nine mongrel clogs, atrial pacing was compared to AV synchronous pacing at three different A V delays (150, 100, and 60 nis). In six dogs, proximal septal AV synchronous pacing was compared to apical A V synchronous pacing at three different A V delays. AV synchronous pacing was performed after RF induced complete heart block. Hemodynarnics were evaluated by assessment of positive and negative dP/dt, cardiac output, and left ventricular and pulmonary pressures. Atrial pacing was superior to AV synchronous pacing with respect to positive and negative dP/dt and cardiac output. This difference was present at all AV delays. Proximal septal pacing was associated with a higher positive and negative dP/dl compared to apical pacing at all AV delays. Left ventricular activation time was significantly shorter during proximal septal pacing than during apical pacing (88 ± 4 vs 115 ± 4 ms, P < 0.001). We conclude that atrial and proximal septal pacing improves cardiac function and shortens the ventricular activation time compared to apical AV synchronous pacing independent of the AV interval.

Prospective study of left ventricular function after radiofrequency ablation of atrioventricular junction in patients with atrial fibrillation.

BACKGROUND--In patients with drug resistant incessant supraventricular tachycardia, radiofrequency induced ablation of the atrioventricular junction and pacemaker implantation have hitherto been considered a treatment of last resort. OBJECTIVE--To assess the short and long term effects of ablation of the atrioventricular junction on systolic and diastolic left ventricular function in patients with atrial fibrillation with and without impaired left ventricular function. PATIENTS--29 patients (19 men; mean age 65 (SD 7) years (range 50-76)) undergoing ablation of the atrioventricular junction for drug refractory atrial fibrillation were examined a mean of 2, 65, and 216 days after ablation of the bundle of His. MAIN OUTCOME MEASURES--Left ventricular ejection fraction and early filling deceleration times (Edec) were assessed by Doppler echocardiography after 1 to 2 hours of ventricular pacing at a rate of 80 beats/minute. RESULTS--In 14 patients with a left ventricular ejection fraction < 50% left ventricular ejection fraction increased significantly from 32% (11%) to 39% (11%) (65 days) and 45% (11%) (216 days) (P < 0.001); Edec increased from 142 (46) ms to 169 (57) ms (65 days) and 167 (56) ms (216 days) (P < 0.05). In 15 patients with an ejection fraction > or = 50% at the initial examination no significant change in systolic function was observed. CONCLUSIONS--In patients with left ventricular dysfunction long term improvement of systolic and diastolic left ventricular function was seen after ablation of the atrioventricular junction for rate control of atrial fibrillation. This procedure had no adverse effects on normal left ventricular function.

Left ventricular hypertrophy in hypertension: its arrhythmogenic potential

Left ventricular (LV) hypertrophy may reflect physiological adaptation to an increased work load of the heart following intense physical training. However, LV hypertrophy often represents a pathophysiologic condition, and can develop due to intrinsic stimuli (cardiomyopathy), or secondary to extrinsic stimuli, such as pressure or volume overload accompanying hypertension and valvar disease (fig 1). Myocardial hypertrophy is also part of the remodelling process following an acute myocardial infarction, and is a common finding in patients with congestive heart failure caused by systolic and/or diastolic LV dysfunction. Figure 1  Left ventricular hypertrophy, a condition with variable background. AMI, acute myocardial infarction; CMP, cardiomyopathy. The presence of LV hypertrophy is a strong independent risk factor for future cardiac events and all cause mortality.1 The risk for sudden cardiac death is increased in subjects with LV hypertrophy, independent of the aetiology, and this event occurs also in individuals with no or only mild prior symptoms related to cardiovascular disease. Intense animal and human research has identified some common features and provided a framework within which some crucial components can be explained. Thus, whether the focus is haemodynamic or electrophysiologic, there seems to be consensus as to the initiation of a fetal-like gene programme in myocardial hypertrophy.2,3 The insights into its consequences can be applied in the clinical management of individual patients. During recent years, experts with different backgrounds within cardiovascular medicine have aimed to create a united picture of cardiac hypertrophy and sudden cardiac death, and to present it in such a way that in can be integrated and applied into clinical cardiovascular practice. This article is an attempt to pursue this ambition. We focus on LV hypertrophy in human hypertension as a model of cardiac hypertrophy, and myocardial hypertrophy as a condition with “reduced repolarisation reserve”,w1 and thus a latent …

Electrophysiologic effects and clinical hazards of carbamazepine treatment for neurologic disorders in patients with abnormalities of the cardiac conduction system

Carbamazepine, a first-line drug for the treatment of epilepsy and neuralgia, may exert hazardous effects on the cardiac conduction system. Standard ECG and long-term ECG monitoring and invasive electrophysiologic testing were carried out in 10 patients who required this drug for neurologic disorders, but in whom its safe use had been questioned because of symptoms of ECG abnormalities. We observed depression of sinus node function and an atrioventricular conduction delay with a significant prolongation of the PQ interval of 16 msec (9%; 95% confidence interval: 1.9% to 16.5%; p less than 0.05), of which the HV interval was significantly prolonged but not the PA and AH intervals. These effects are in accordance with previously shown class 1A properties. However, the lack of effects on QRS, JT, and QT intervals at normal heart rates is a class 1B characteristic. Thus carbamazepine seems to have composite electropharmacologic actions. A cause effect relationship between carbamazepine treatment and significant arrhythmias was established in five patients. Thus the negative chronotropic and dromotropic effects of carbamazepine may, at least in predisposed patients, induce symptoms confusingly similar to the epileptic seizures it is used to prevent.

Diagnostic value of programmed ventricular stimulation in patients with bifascicular block: A prospective study of patients with and without syncope

OBJECTIVES The aim of this study was to examine the inducibility of ventricular arrhythmias in patients with bifascicular block both with and without a history of syncope and to relate the findings to clinical events during follow-up. BACKGROUND Patients with bifascicular block have an increased risk of sudden death that is not reduced by pacemaker treatment. This risk could be related to a high incidence of ventricular arrhythmias. METHOD Programmed ventricular stimulation was performed in 101 patients with bifascicular block: 41 had a history of unexplained syncope, and 60 were asymptomatic. RESULTS Programmed ventricular stimulation resulted in a sustained ventricular arrhythmia in 18 patients (18%), 8 in the syncope group and 10 in the nonsyncope group (p = NS). Three patients in each group had an inducible sustained monomorphic ventricular tachycardia. During a mean follow-up of 21 months, 10 patients experienced a clinical event defined as sudden death (n = 4), syncope (n = 5) or appropriate discharges from an implantable cardioverter-defibrillator (n = 1). Only one of these patients had an inducible ventricular arrhythmia at baseline. CONCLUSIONS The inducibility of ventricular arrhythmias is high in patients with bifascicular block and of the same magnitude in patients with and without a history of syncope. Clinical events during follow-up were not predicted by programmed ventricular stimulation in either of the two groups. The finding of inducible ventricular arrhythmia in patients with bifascicular block should therefore be interpreted with caution.

Myocardial Injury After Electrical Therapy for Cardiac Arrhythmias Assessed by Troponin-T Release

Episodes of ventricular fibrillation with subsequent intracardiac, and to a lesser extent, external defibrillation give rise to a statistically significant increase in S-troponin T, S-CK-MB(mass) and S-myoglobin indicative of a minor myocardial injury or dysfunction. In contrast, no such signs were observed after external direct-current conversion of atrial fibrillation using high energies, or after pace-terminated ventricular tachycardia.

Changes in arrhythmia profile and heart rate variability during abrupt withdrawal of antiepileptic drugs. Implications for sudden death

Sudden unexpected death (SUD) has been associated with low or undetectable concentrations of antiepileptic drugs in patients with epilepsy suggesting that a sudden fall in plasma levels of these drugs might be a critical factor for the occurrence of SUD. We studied the changes in arrhythmia profile and heart-rate variability, during abrupt withdrawal of carbamazepine and phenytoin treatment in 10 patients with side effects on these drugs. Continuous ECG recording and daily measurements of drug plasma concentrations were performed from the last day of steady-state treatment and the following 4 days. Three patients had a 10-fold increase in ventricular premature beats. In addition, there was a significant reduction in heart-rate variability, assessed over 24 hours, in both the time (SDNN index, P = 0.03) and frequency domains from days 1-5. In the frequency domain analysis there was a significant reduction in total power (P = 0.01), very-low-frequency power (P = 0.004) and in low-frequency (LF) power (P = 0.01). Similar reductions in heart-rate variability and increases in ventricular automaticity have been associated with increased mortality in other patient groups. Two factors that might contribute to the increased rate of SUD in patients with epilepsy have thus been identified.

Changes in ventricular repolarization during percutaneous transluminal coronary angioplasty in humans assessed by QT interval, QT dispersion and T vector loop morphology

Abstract. Nowinski K, Jensen S, Lundahl G, Bergfeldt L (Karolinska Hospital, Stockholm, Norrlands University Hospital, Umeå and Ortivus AB, Täby, Sweden). Changes in ventricular repolarization during percutaneous transluminal coronary angioplasty in humans assessed by QT interval, QT dispersion and T vector loop morphology. J Intern Med 2000; 248: 126–136.

HLA-B27: An important genetic risk factor for lone aortic regurgitation and severe conduction system abnormalities

PURPOSE HLA-B27, an immunogenetic marker that is present in 8 percent of the white population around the world, has been found to be an important risk factor for the development of a group of rheumatic disorders, the seronegative spondyloarthropathies. Our objective was to assess the possible role of HLA-B27 and the associated inflammatory disease process in the development of lone aortic regurgitation. PATIENTS AND METHODS A group of 91 patients with lone aortic regurgitation were studied by HLA typing and clinical and roentgenologic examination. RESULTS The HLA-B27-associated inflammatory disease process was found to be the probable underlying cause in 15 to 20 percent of patients with lone aortic regurgitation of different degrees of severity. Furthermore, HLA-B27 was found in 88 percent of the male patients with the combination of aortic regurgitation and severe conduction system abnormalities. CONCLUSION We suggest that this cardiac syndrome should be regarded as an HLA-B27-associated syndrome, sometimes part of ankylosing spondylitis or Reiters disease, but just as often presenting without obvious rheumatic disease. The marker is thus an important and widely distributed risk factor not only for the development of rheumatic disease but also for acquired aortic regurgitation and sever conduction system abnormalities.

Ankylosing spondylitis: An important cause of severe disturbances of the cardiac conduction system: Prevalence among 223 pacemaker-treated men☆

The cause of severe disturbances of the cardiac conduction system is seldom possible to establish clinically at pacemaker implantation, apart from cases of acute myocardial infarction or digitalis intoxication and in relatively rare cases of inflammatory disorders such as sarcoidosis and systemic sclerosis. Since cardiac manifestations, mainly conduction disturbances, occur in patients with ankylosing spondylitis, the prevalence of this disease was determined using radiologic screening for sacroiliitis in a population of 223 men who had permanently implanted pacemakers. Sacroiliitis was found in 19 men (8.5 percent), 15 of whom fulfilled the diagnostic criteria for ankylosing spondylitis. In six patients, sacroiliitis was asymptomatic and two of the patients were completely free of symptoms other than those originating from their heart manifestations. In seven of the 15 patients with ankylosing spondylitis and in the four patients with sacroiliitis without clinical criteria of ankylosing spondylitis, the diagnosis was previously unknown. Uveitis and aortic regurgitation occurred in five patients each, while peripheral arthritis was twice as common. The prevalence of sacroiliitis and ankylosing spondylitis of 8.5 and 6.7 percent, respectively, differ significantly (p less than 0.01) from the frequencies found in general Caucasian populations of 1 to 2 and 0.1 to 0.5 percent, respectively. HLA B27 was present in more than 80 percent of the patients with sacroiliitis and/or ankylosing spondylitis, compared with 8 to 10 percent in the general population. This strong association is in accordance with previous studies of patients with symptomatic sacroiliitis and/or ankylosing spondylitis. Thus sacroiliitis, diagnosed by x-ray, can be considered a marker for this relatively common rheumatic cause of severe disturbances of the cardiac conduction system.