Left ventricular conduction delays induced by right ventricular apical pacing: effect of left ventricular dysfunction and bundle branch block

Background: RV apical pacing (RVP) may be deleterious, possibly by simulating LBBB, i.e., prolonging QRS duration (QRSd) and LV activation (LVAT). However, determinants of electrical delays are unknown.
Hypothesis: LV dysfunction (LVEF ≤ 40%, HF) and pre-existing conduction system abnormalities may modulate RVP's effects, compared to LBBB.
Methods: RVP-induced QRSd and LVAT were compared in normal LV to HF, with normal QRS (<120 ms), RBBB, or LBBB. LVAT was estimated by interval from QRS onset to basal inferolateral LV depolarization.
Results: During LBBB and RVP, LVAT/QRSd was ≥85%, i.e., LVAT indicated terminal LV depolarization. In normal LV, LVAT during intrinsic conduction (55 ± 18 ms) was delayed by RVP (129 ± 20 ms, n = 58, P < 0.001). RVP's effects were similar to LBBB (P = NS) and unaffected by baseline conduction disease. In HF overall, RVP-induced delays (QRSd 209 ± 27, LVAT 186 ± 26 ms, n = 102) were greater than RVP in normal LV (P < 0.001). When baseline conduction system disease was present, RVP's effects were exaggerated (RVP wide QRS [>120 ms]: QRSd 216 ± 27, LVAT 191 ± 20 ms, [n = 72] vs RVP normal QRS: QRSd 193 ± 24, LVAT 169 ± 24 ms, n = 31, P < 0.001). In patients with LBBB (n = 41), delays during intrinsic conduction (QRSd 163 ± 29, LVAT 137 ± 33 ms, n = 41) were enhanced by RVP (QRSd 218 ± 28, LVAT 191 ± 22 ms, P < 0.001). RVP's effects were similar in patients with LBBB and RBBB (P = NS).
Conclusion: RVP simulated LBBB in normal LV. In HF, RVP induced greater conduction delays than LBBB, enhanced by accompanying conduction disease. These variations may contribute to RVP's mixed clinical effects.     

Traumatic heart block and tachyarrhythmia induced by right ventricular impact

The effect of direct impact on the right ventricle was investigated in an anesthetized open-chest canine preparation. At each of five impact sites, direct local loading produced immediate ventricular asystole followed by varying degrees of AV conduction block, lasting 70 +/- 35 seconds. Sinus rhythm temporarily resumed in most cases for 30 +/- 25 seconds before ventricular tachycardia abruptly intervened for 150 +/- 70 seconds. Recovery to sinus rhythm usually followed the ventricular tachycardia. Impact over the ventricular aspect supplied by the right coronary artery above the conduction bundle branches caused a longer period of asystole than impact over other sites. The duration of the delayed tachyarrhythmia was independent of impact site. Denervation of the heart did not influence the conduction block or the tachyarrhythmia. Intravenous injection of propranolol (1.6 mg/kg) did not affect the immediate conduction block but prevented the ventricular tachycardia.     

Left ventricular involvement in right ventricular dysplasia.

Right ventricular dysplasia, a heart muscle disease of unknown cause, anatomically characterized by variable replacement of myocardial muscle with adipose or fibroadipose tissue, is usually considered a selective disorder of the right ventricle. However, concomitant left ventricular involvement has been noted in a few cases. The aim of this study was to evaluate the prevalence and characteristics of left ventricular involvement in right ventricular dysplasia, as well as possible progression of the disease. Thirty-nine patients with right ventricular dysplasia were studied by M-mode and two-dimensional echocardiography; 28 of them also underwent cardiac catheterization, and in 25 endomyocardial biopsy was performed. On first examination the left ventricle was normal in 25 patients, whereas in the remaining 14 right ventricular abnormalities were associated with left ventricular involvement, characterized by asynergic areas (12 patients) or diffuse mild hypokinesis (two patients). During follow-up (27 patients, 84.1 +/- 66.1 months) 10 patients showed worsening of right ventricular function; in nine the appearance or worsening of left ventricular abnormalities was observed. Five patients died (four in congestive heart failure and one suddenly). Results of postmortem examination (available in two patients) showed atrophy of myocells and a massive fatty and fibrous infiltration of the right ventricular wall, associated with degenerative changes and fibrosis of the left ventricle. In conclusion, right ventricular dysplasia may be associated with left ventricular involvement and the disorder appears to be progressive in some instances.     

Myocardial collagen, the effects of right ventricular hypertrophy and its involution induced by changes in atmospheric pressure.

Right ventricular hypertrophy induced by hypobaric conditions was accompanied by an increased collagen mass. Left ventricular collagen was unaffected. Right ventricular mass remained unchanged after involution of right ventricular hypertrophy on return to normobaric conditions. Dietary restriction limited the size and collagen mass of both ventricles.     

Left atrial abnormality by electrocardiogram predicts left ventricular hypertrophy by echocardiography in the presence of right bundle-branch block

Background: Left ventricular hypertrophy (LVH) on the electrocardiogram (ECG) may be masked in the presence of complete right bundle-branch block (RBBB). Left bundle-branch block on the ECG is associated with LVH at autopsy in 93% of hearts studied. However, RBBB does not predict LVH and the usual ECG criteria applied for LVH may not be reliable in the presence of RBBB. Hypothesis: The study was undertaken to evaluate left atrial (LA) abnormality as a criterion for the diagnosis of LVH in the presence of RBBB. Methods: Left atrial abnormality in the ECG was assessed by two independent observers as a criterion of LVH in the presence of RBBB in 100 patients, and data were compared with those of 50 patients without LA abnormality. Results: Left ventricular hypertrophy was confirmed by echocardiographic determination of left ventricular (LV) mass in both groups. Observers reliably differentiated between hy-pertrophied and normal-sized LV in the presence of RBBB by using LA abnormality as an ECG criterion when correlated with LV mass determined by echocardiography. Observer 1 correctly detected LVH in 88% and Observer 2 in 82% of patients. False positive diagnosis was made in 12 and 18% of patients by Observers 1 and 2, respectively. Observers' performance of recognition of LA abnormality in the present study was 94%. Results showed sensitivity of 76 and 70% and specificity of 84 and 92% for Observers 1 and 2, respectively. Left ventricular mass increased significantly and was diagnostic of LVH in 92% of patients with LA abnormality. Left ventricular mass was high in 84% of patients when corrected by body surface area. LVH in the presence of RBBB by the ECG was found in only seven patients (5%) when six commonly used conventional criteria of diagnosis of LVH by ECG were employed. Regression analysis found LA abnormality to be a strong independent predictor of increased LV mass. Multiple regression analysis revealed that age, body mass index, body surface area, and frontal axis are also significant predictors of LV mass. Conclusion: The results obtained by the correlation of LA abnormality by ECG and LVH by echocardiography conclude that LA abnormality by ECG was significantly diagnostic of LV hypertrophy in the presence of RBBB.     

Left ventricular ejection and ejection reserve during isoproterenol infusion in hypertrophic obstructive cardiomyopathy (author's transl)]

In 10 patients with hypertrophic obstructive cardiomyopathy (HOCM) and in 10 patients without heart disease (normals) left ventricular function and myocardial reserve under isoproterenol (Iso) infusion (0.3 microgram/kg B.W./min) were measured. From the monoplane cineangiography of the left ventricle diastolic wall thickness as well as ejection phase contractile indices, ejection fraction (EF) mean velocity of fiber shortening (VCF) and mean normalized systolic ejection rate (MNSER), were calculated. Maximum total load (TL) served as measure for afterload. Wall thickness in HOCM was higher by 73% as compared to normals (p less than 0.001). Hemodynamic values for normals at rest were as follows: EF 68.9 +/- 8.0%, VCF 1.22 +/- 0.19 circ/sec, MNSER 2.25 +/- 0.25 vol/sec and TL 228.6 +/- 37.4 dynes . 10(5). Values for HOCM at rest were as follows: EF 77.4 +/- 7.71% (p less than 0.05), VCF 1.53 +/- 0.3 circ/sec (p less than 0.05); MNSER 2.66 +/- 0.35 vol/sec (p less than 0.01) and TL 288.5 +/- 55.5 dynes . 10(5) (p less than 0.01) as compared to normals. The values under Iso in normals resulted in a significant fall of the TL (p less than 0.05), the enddiastolic volume (EDV, p less than 0.05) and of the enddiastolic pressure (EDP, p less than 0.05), VCF rose by 89% (p less than 0.001), MNSER by 66% (p less than 0.001) and EF by 23% (p less than 0.001). In HOCM under Iso TL rose by 45% (p less than 0.05), EDV and EDP did not change (p less than 0.05), VCF and MNSER rose by 23% (p less than 0.05 respectively p less than 0.01). VCF and MNSER in HOCM with Iso were reduced by 17% respectively by 13% (p less than 0.01) as compared to normals, the EDP was increased by factor 4, while EDV showed no significant difference (p less than 0.05). Our results indicate that the left ventricle in HOCM in spite of its marked hypertrophy is unable to adequately compensate for an acute gain of afterload as induced by the effect of catecholamines. Therefore, we assume stress-related congestive symptoms in HOCM to be caused--aside from other mechanisms--by diminished ejection reserve.     

Intermittent pseudocomplete A-V block due to A-V dissociation in presence of 2:1 A-V block.

A false pattern of intermittent complete A-V block was seen in two asymptomatic patients when A-V dissociation was superimposed on a basic 2:1 A-V block. Although the conduction disturbance occurred at the A-V nodal level in both cases, in Case 2 it resembled A-V block due to bilateral or trifascicular disease. This arrhythmia was the end result of Type I (Wenckebach) block and apparently has a better prognosis than those emerging from a Type II (Mobitz) block.     

Left ventricular volumes and functioning of the reindeer heart

Summary Left ventricular volumes were measured by cineangiocardiography in 56 sessions on 25 reindeer, together with determinations of arterial pressure and blood oxygen saturation.The heart rate with the animal kept lying on the sternum at rest was 50 b/ min the aortic blood oxygen saturation 94 to 98% and the aortic blood pressure 153/130/115 mm Hg. The left ventricular end-diastolic volume was 3.4 ml/kg of b.w., stroke volume 2.6 ml/kg, cardiac output 133 ml/kg·min, and ejection fraction 76%. If the animal was placed on its side the aortic blood oxygen saturation decreased by 2 to 3 per cent, end-diastolic volume rose 10%, stroke volume 25%, cardiac output nearly 30% and ejection fraction 14%.The heart rate and cardiac output increased in hypoxemia, but the enddiastolic and stroke volumes simultaneously decreased. If the aortic blood pressure rose during hypoxia, the end-diastolic and stroke volumes increased, while the ejection fraction first increased and then decreased again.In normoxia a rise in aortic blood pressure was associated with decreased end-diastolic and stroke volumes and ejection fraction. An increased heart rate at rest was followed by increased cardiac output, but decreased end-diastolic and stroke volumes and ejection fraction.

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Teilvolumina des linken Ventrikels und Arbeitsweise des Rentierherzens

Zusammenfassung Bei 25 Rentieren wurde das Innenvolumen des linken Ventrikels mit Hilfe einer kineangiokardiographischen Methode in 56 Sitzungen gemessen. Gleichzeitig wurden der arterielle Blutdruck und die Sauerstoffsättigung des Blutes bestimmt.Beim ruhenden, auf dem Sternum liegenden Tier betrug die Herzfrequenz 50 Schläge/min, die Sauerstoffsättigung der Aorta 94 bis 98% und der Aortendruck 153/130/115 mm Hg. Das enddiastolische Volumen betrug 3,4 ml/kg, das Schlagvolumen 2,6 ml/kg, das Herzminutenvolumen 133 ml/kg und die Austreibungsfraktion 76%. Beim Tier in Seitenlage war die Sauerstoffsättigung der Aorta um 2 bis 3% vermindert, das enddiastolische Volumen um 10%, das Schlagvolumen um 25%, das Herzminutenvolumen beinahe um 30% und die Austreibungsfraktion um 14% erhöht.Bei gesteigertem Aortendruck waren Schlagvolumen, enddiastolisches Volumen und Austreibungsfraktion bei Normoxie vermindert, während unter Hypoxie das enddiastolische Volumen und das Schlagvolumen erhöht, die Austreibungsfraktion zunächst erhöht und danach vermindert waren. Unter Hypoxie nahmen Herzfrequenz und Herzminutenvolumen zu bei gleichzeitigem Rückgang von enddiastolischem Volumen und Schlagvolumen. Eine erhöhte Herzfrequenz ohne Muskelarbeit führte zu einer Steigerung des Herzminutenvolumens, während enddiastolisches Ventrikelvolumen, Schlagvolumen und Austrebungsfraktion gleichzeitig vermindert waren.

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With 4 figures and 2 tables