Left ventricular myocardal activation under ventricular paced beats in chickens Gallus gallus domesticus

The aim of the study was to advance our knowledge regarding the activation process of the ventricular myocardium in birds in which Purkinje fibres penetrate into the ventricular wall to reach the epicardium. A depolarization pattern of the left ventricular free wall was studied in chickens (Gallus gallus) during ventricular paced beats. Duration of the activation process of the left ventricular free wall is significantly increased during ventricular ectopic excitation as compared with sinus rhythm. Its lowest increase occurs during subendocardial pacing of the middle part of the left ventricle, but its greatest increase is observed during subepicardial pacing of the left ventricular base. Multifocality and mosaicity of depolarization of the left ventricular free wall myocardium in chicken are expressed in a considerably less degree during ventricular paced beats in comparison with sinus rhythm. During ventricular paced beats, excitation of the left ventricular free wall is mostly due to the successive spreading of the depolarization wave from pacing sites.     

Left ventricular false tendons

Left ventricular false tendons (LVFTs) are fibromuscular structures, connecting the left ventricular free wall or papillary muscle and the ventricular septum.There is some discussion about safety issues during intense exercise in athletes with LVFTs, as these bands have been associated with ventricular arrhythmias and abnormal cardiac remodelling. However, presence of LVFTs appears to be much more common than previously noted as imaging techniques have improved and the association between LVFTs and abnormal remodelling could very well be explained by better visibility in a dilated left ventricular lumen.Although LVFTs may result in electrocardiographic abnormalities and could form a substrate for ventricular arrhythmias, it should be considered as a normal anatomic variant. Persons with LVFTs do not appear to have increased risk for ventricular arrhythmias or sudden cardiac death.     

Impaired left ventricular filling due to right-to-left ventricular interaction in patients with pulmonary arterial hypertension

The aim of this study was to investigate the contribution of direct right-to-left ventricular interaction to left ventricular filling and stroke volume in 46 patients with pulmonary arterial hypertension (PAH) and 18 control subjects. Stroke volume, right and left ventricular volumes, left ventricular filling rate, and interventricular septum curvature were measured by magnetic resonance imaging and left atrial filling by transesophageal echocardiography. Stroke volume, left ventricular end-diastolic volume, and left ventricular peak filling rate were decreased in PAH patients compared with control subjects: 28 +/- 13 vs. 41 +/- 10 ml/m(2) (P < 0.001), 46 +/- 14 vs. 61 +/- 14 ml/m(2) (P < 0.001), and 216 +/- 90 vs. 541 +/- 248 ml/s (P < 0.001), respectively. Among PAH patients, stroke volume did not correlate to right ventricular end-diastolic volume or mean pulmonary arterial pressure but did correlate to left ventricular end-diastolic volume (r = 0.62, P < 0.001). Leftward interventricular septum curvature was correlated to left ventricular filling rate (r = 0.64, P < 0.001) and left ventricular end-diastolic volume (r = 0.65, P < 0.001). In contrast, left atrial filling was normal and not correlated to left ventricular end-diastolic volume. In PAH patients, ventricular interaction mediated by the interventricular septum impairs left ventricular filling, contributing to decreased stroke volume.     

Left ventricular noncompaction cardiomyopathy

Isolated left ventricular noncompaction (ILVNC) is a congenital abnormality in the structure of ventricular tissue due to amorphogenetic defect during embryogenesis. This rare entity can be easily diagnosed by the characteristic appearance of prominent trabeculations and deep inter-trabecular spaces. Clinical manifestations of this disease include benign and malignant ventricular arrhythmia, congestive heart failure signs, cardio-embolic events (stroke), mitral and pulmonary valve incompetence, and reduced global ventricular systolic function. We present the case report of a 58-year-old man with ILVNC.     

Left ventricular effects on right ventricular developed pressure.

The possibility that left ventricular (LV) performance might affect right ventricular (RV) function through the myocardium was examined by using isolated, flow-perfused, paced rabbit hearts beating isovolumically. Reducing LV volume from its optimal volume to zero caused a 5.7% decrease (N = 10, P less than 0.001) in right ventricular developed pressure (RVDP). Ligating the anterior ventricular branches of the left coronary artery which in the rabbit supply the LV free wall resulted in an additional 9.3% decrease in RVDP (N = 5, P = 0.05) within 3 min of ligation. Finally, cutting the LV free wall from the atrioventricular orifice to the apex (thereby preventing any developed LV free wall force during systole) caused a 45% further decrease in RVDP (N = 2, P less than 0.02). Cineradiographic study showed that the alterations in RVDP resulting from changes in LV volume and coronary occlusion correlated significantly (N = 5, P less than 0.01) with the magnitude of septal bulging into the RV cavity during systole. The results indicate that alteration in LV free wall function and changes in LV volume can directly effect RVDP through the myocardium.     

Redistribution in left ventricular regional flow following acute right ventricular pressure overload

The left ventricular dysfunction following acute pulmowary hypertension remains unexplained. We wondered if acute pulmonary hypertension could alter the transmural flow distribution within the left ventricular myocardium, independent of coronary flow and perfusion pressure. We used a canine preparation in which the left coronary system was perfused at constant flow and induced a two- to three-fold increase in pulmonary artery pressure by banding the pulmonary artery. Regional myocardial blood flow of the left coronary system was measured using radioactive microspheres, injected into the left coronary system before and after 10-30 min of banding of the pulmonary artery. The left ventricular subendocardial:epicardial ratio fell by 12 and 31% (p less than 0.05) of control value, 10 and 30 min, respectively, after banding of the pulmonary artery, the total flow to the left coronary system being kept constant. Left atrial mean pressure increased from 2.9 +/- 2.4 to 3.6 +/- 1.9 and 6.0 +/- 2.1 (p less than 0.05) following banding. The mechanism of the redistribution of coronary flow may relate to inappropriate vasodilation of the right septal myocardium with consequent relative left ventricular subendocardial hypoperfusion which might aggravate left ventricular ischemia in the presence of hypotension and hypoxia.     

Arrhythmogenic right ventricular cardiomyopathy/dysplasia

Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is a heart muscle disease clinically characterized by life-threatening ventricular arrhythmias. Its prevalence has been estimated to vary from 1:2,500 to 1:5,000. ARVC/D is a major cause of sudden death in the young and athletes. The pathology consists of a genetically determined dystrophy of the right ventricular myocardium with fibro-fatty replacement to such an extent that it leads to right ventricular aneurysms. The clinical picture may include: a subclinical phase without symptoms and with ventricular fibrillation being the first presentation; an electrical disorder with palpitations and syncope, due to tachyarrhythmias of right ventricular origin; right ventricular or biventricular pump failure, so severe as to require transplantation. The causative genes encode proteins of mechanical cell junctions (plakoglobin, plakophilin, desmoglein, desmocollin, desmoplakin) and account for intercalated disk remodeling. Familiar occurrence with an autosomal dominant pattern of inheritance and variable penetrance has been proven. Recessive variants associated with palmoplantar keratoderma and woolly hair have been also reported. Clinical diagnosis may be achieved by demonstrating functional and structural alterations of the right ventricle, depolarization and repolarization abnormalities, arrhythmias with the left bundle branch block morphology and fibro-fatty replacement through endomyocardial biopsy. Two dimensional echo, angiography and magnetic resonance are the imaging tools for visualizing structural-functional abnormalities. Electroanatomic mapping is able to detect areas of low voltage corresponding to myocardial atrophy with fibro-fatty replacement. The main differential diagnoses are idiopathic right ventricular outflow tract tachycardia, myocarditis, dialted cardiomyopathy and sarcoidosis. Only palliative therapy is available and consists of antiarrhythmic drugs, catheter ablation and implantable cardioverter defibrillator. Young age, family history of juvenile sudden death, QRS dispersion ≥ 40 ms, T-wave inversion, left ventricular involvement, ventricular tachycardia, syncope and previous cardiac arrest are the major risk factors for adverse prognosis. Preparticipation screening for sport eligibility has been proven to be effective in detecting asymptomatic patients and sport disqualification has been life-saving, substantially declining sudden death in young athletes.     

Electrical requirements for ventricular defibrillation.

Most deaths from ischaemic heart disease are sudden, occur outside hospital, and result from ventricular fibrillation. But defibrillators have only limited availability because of their size and weight. A miniature defibrillator has been developed. A singe low-energy shock succeeded in removing ventricular fibrillation in 73 out of 82 episodes, and a further shock was successful in seven more episodes. Primary ventricular fibrillation probably always responds to low-energy electrical shocks, which challenges the conventional view that correction of ventricular fibrillation requires high-energy direct-current shock. Thus even smaller and lighter defibrillators are possible. Furthermore low-energy shocks cause less myocardial damage.     

Passive ventricular constraint

Heart failure (HF) is a progressive degenerative and malignant syndrome with a large number of aetiologies including coronary artery disease, chronic hypertension, exposure to toxins, bacteria and viruses and in a significant percentage of HF patients, the causal mechanism is unclear. The HF trail of morbidity and mortality is well documented and is characterised by step-like periods of relative symptomatic stability, compensation, separated by decompensatory episodes. The homeostatic response to the decline in cardiac function is diverse and involves most organs. There is an increase in resting rate, intra-cardiac hormone production (catecholamines, aldosterone, etc.) and in particular structural changes occur with increased mass and dilatation (dilated cardiomyopathy, DCM). DCM is associated with decreased cardiac output, contractility and energy efficiency and an increase in pro-arrhythmia and conduction defects.

Kass et al. (Circulation 91(9) (1995) 2314) first demonstrated in patients who had undergone a dynamic cardio-myoplasty procedure, that, preventing further dilatation in DCM was beneficial and that the improved cardiovascular status was largely independent of muscle stimulation. We hypothesised that this outcome could be achieved by implanting a fabric cardiac support device around both ventricles to the AV junction. Subsequently, it was shown by us and others (Kass et al., 1995) (Cardiovasc. Res. 44(3) (1999) 549); (Ann. Thorac. Surg. 70(4) (2000) 1275) (in different animal models of DCM) that passive ventricular constraint prevented further dilatation, initiated left ventricular volume reduction and reversed the decline in ejection fraction, mitral valve integrity and left ventricular contractility, when compared with untreated controls. Subsequent European and North American clinical trials in patients with DCM of varying aetiologies have shown equal promise and an absence of device related complications (Circulation 104(12 Suppl. 1) (2001) I270); (Ann. Thorac. Cardiovasc. Surg. 7(5) (2001) 278).

The mechanisms behind this improvement have yet to be fully clarified however the support generated by the device upon the right and ventricular freewall would lower wall tension.

Not only is passive ventricular constraint a very promising treatment modality for heart failure and DCM it should provide a useful research tool for the study of the role of ventricular dilatation in the progression of heart failure.     

Idiopathic submitral left ventricular aneurysm: an unusual substrate for ventricular tachycardia in Caucasians

Annular submitral aneurysms have been rarely reported in Caucasians. They are typically diagnosed in non-white adults who present with severe mitral regurgitation, heart failure, systemic embolism, ventricular arrhythmias, and sudden cardiac death. In this article, we describe the case of a white woman, presenting with ventricular tachycardia, who had a large submitral left ventricular aneurysm diagnosed incidentally during coronary angiography.     

Right and left ventricular pressure-volume response to respiratory maneuvers

With respiration, right ventricular end-diastolic volume fluctuates. We examined the importance of these right ventricular volume changes on left ventricular function. In six mongrel dogs, right and left ventricular volumes and pressures and esophageal pressure were simultaneously measured during normal respiration, Valsalva maneuver, and Mueller maneuver. The right and left ventricular volumes were calculated from cineradiographic positions of endocardial radiopaque markers. Increases in right ventricular volume were associated with changes in the left ventricular (LV) pressure-volume relationship. With normal respiration, right ventricular end-diastolic volume increased 2.3 +/- 0.7 ml during inspiration, LV transmural diastolic pressure was unchanged, and LV diastolic volume decreased slightly. This effect was accentuated by the Mueller maneuver; right ventricular end-diastolic volume increased 10.4 +/- 2.3 ml (P less than 0.05), while left ventricular end-diastolic pressure increased 3.6 mmHg (P less than 0.05) without a significant change in left ventricular end-diastolic volume. Conversely, with a Valsalva maneuver, right ventricular volume decreased 6.5 +/- 1.2 ml (P less than 0.05), and left ventricular end-diastolic pressure decreased 2.2 +/- 0.5 mmHg (P less than 0.05) despite an unchanged left ventricular end-diastolic volume. These changes in the left ventricular pressure-volume relationship, secondary to changes in right ventricular volumes, are probably due to ventricular interdependence. Ventricular interdependence may also be an additional factor for the decrease in left ventricular stroke volume during inspiration.     

An inappropriate defibrillator shock during ventricular tachycardia

Ventricular oversensing in patients with defibrillators is an infrequent but deleterious condition. We report a patient with a cardiac resynchronization–defibrillation device that presented with hyperkalemia and syncope. Device interrogation revealed ventricular double-counting within the QRS of a slow ventricular tachycardia, resulting detection of the slow ventricular tachycardia in the ventricular fibrillation zone, and delivery of an effective therapy, below device programmed detection rate. This case of defibrillator inappropriate detection emphasizes the relevance of device electrogram interrogation in order to minimize inappropriate therapies.     

Localized endocrine conversion of ventricular cardiocytes in ventricular aneurysm

Atrial natriuretic peptide (ANP) is synthesized and stored in the atria of the heart, but not or at very low concentrations in the ventricles. We investigated the occurrence of ANP and its messenger RNA (mRNA) in human ventricular aneurysm where the cardiocytes were physically over-stretched. The techniques of light and electron microscopic immunocytochemistry, and RNA-RNA tissue in situ hybridization were employed. A large amount of ANP immunoreactivity was found in the cytoplasm of the cardiocytes in and around the aneurysm, but not in fibrous scar tissue or in the normal ventricles. Immunoelectron microscopy localized the immunoreactivity mainly to specific secretory granules in the cytoplasm of the cardiocytes. ANP mRNA was also detected in these cardiocytes. The abundance of both was much higher than that found in the hypertrophic ventricles of other types. The highest concentration of ANP immunoreactivity and of ANP mRNA was found in the cardiocytes located at the border zone. The quantities of both ANP and its mRNA decreased in cardiocytes more distant from the lesion. Our findings suggest that human ventricular cardiocytes in and around aneurysm can convert to produce large amounts of the endocrine peptide ANP. This ventricular endocrine conversion was localized and was probably caused by physical over-stretch of the cardiocytes.     

Right ventricular TNF resistance during endotoxemia: the differential effects on ventricular function

Right and left ventricular myocytes originate from different cellular progenitors; however, it is unknown whether these cells differ in their response to endotoxemia. We hypothesized that 1) the percentage of endotoxemic functional depression within the right ventricle (RV) would be smaller than that of the left ventricle; and 2) that better RV function would correlate with lower levels of right ventricular TNF production. Adult Sprague-Dawley rats were divided into right and left control and endotoxin groups. Controls received vehicle, while endotoxin groups received LPS at 20 mg/kg ip. Hearts were excised either 2 or 6 h after injection. Hearts excised at 2 h were assayed for TNF, IL-6, TNF receptor 1 (TNFR1), TNFR2, and via ELISA, while hearts excised at 6 h were assayed via the Langendorff model. The percentage of cardiac functional depression, exhibited as developed pressure, contractility, and rate of relaxation (expressed as a percentage of control) was significantly smaller in right ventricles compared with left ventricles following endotoxin exposure. Tissue levels of TNF were significantly elevated in both right and left ventricles 2 h after endotoxin exposure, and right ventricular endotoxin groups expressed higher levels of TNF compared with their left ventricular counterparts. No significant differences in IL-6, TNFR1, or TNFR2 levels were noted between endotoxin-exposed ventricles. This is the first study to demonstrate that right and left ventricular function differs after endotoxin exposure.     

Steeper restitution slopes across right ventricular endocardium in patients with cardiomyopathy at high risk of ventricular arrhythmias

Steep action potential duration (APD) restitution slopes (>1) and spatial APD restitution heterogeneity provide the substrate for ventricular fibrillation in computational models and experimental studies. Their relationship to ventricular arrhythmia vulnerability in human cardiomyopathy has not been defined. Patients with cardiomyopathy [left ventricular (LV) ejection fraction <40%] and no history of ventricular arrhythmias underwent risk stratification with programmed electrical stimulation or T wave alternans (TWA). Low-risk patients (n = 10) had no inducible ventricular tachycardia (VT) or negative TWA, while high-risk patients (n = 8) had inducible VT or positive TWA. Activation recovery interval (ARI) restitution slopes were measured simultaneously from 10 right ventricular (RV) endocardial sites during an S1-S2 pacing protocol. ARI restitution slope heterogeneity was defined as the coefficient of variation of slopes. Mean ARI restitution slope was significantly steeper in the high-risk group compared with the low-risk group [1.16 (SD 0.31) vs. 0.59 (SD 0.19), P = 0.0002]. The proportion of endocardial recording sites with a slope >1 was significantly larger in the high-risk patients [47% (SD 35) vs. 13% (SD 21), P = 0.022]. Spatial heterogeneity of ARI restitution slopes was similar between the two groups [29% (SD 16) vs. 39% (SD 34), P = 0.48]. There was an inverse linear relationship between the ARI restitution slope and the minimum diastolic interval (P < 0.001). In cardiomyopathic patients at high risk of ventricular arrhythmias, ARI restitution slopes along the RV endocardium are steeper, but restitution slope heterogeneity is similar compared with those at low risk. Steeper ARI restitution slopes may increase the propensity for ventricular arrhythmias in patients with impaired left ventricular function.     

Radionuclide diagnosis of right ventricular myocardial infarction

The diagnostic capacities of 99mTc-pyrophosphate plane myocardial scintigraphy versus 99mTc-pyrophosphate single photon emission computed tomography (SPECT) were compared. Recording right precordial ECG leads showed that 26 patients had right ventricular myocardial infarction (MI)-typical changes as ST-segment evaluation, followed by abnormal Q wave. Plane scintigraphy indicated a characteristic inclusion of 99mTc-pyrophosphate into the right ventricular myocardium in 18.8% of the patients with acute lower MI and in one of 38 patients with acute MI of the anterior left ventricular wall. SPECT revealed a characteristic inclusion of 99mTc-pyrophosphate into the right ventricular myocardium much more frequently than did plane myocardial scintigraphy--in 34% of cases. Right ventricular myocardial inclusion of 99mTc-pyrophosphate was found in 50% of the patients with acute lower MI, including all 9 patients with positive 99mTc-pyrophosphate myocardial scintigraphy. Thus, the sensitivity of SPECT in the diagnosis of right ventricular MI is somewhat higher than that of precordial ECG and more than thrice higher than that of plane scintigraphy.     

Late elimination of challenging idiopathic ventricular arrhythmias originating from left ventricular summit by anatomical ablation

Ablation of premature ventricular complexes (PVCs) originating from left ventricular outflow tract (LVOT)/left ventricular summit (LVS) is challenging with considerable rate of failure. Recently, in a novel approach to ablation of these arrythmias, application of radiofrequency energy to anatomically opposite sites of presumed origin of arrythmia, has been associated with moderate procedure success. Although late elimination of PVCs that are persistent following an ablation procedure has been previously reported, this observation has not been studied sufficiently. In this report, firstly, we present three cases of lately eliminated LVS PVCs, then, we discuss possible mechanism of this observation and conclude that after an initial failed attempt of anatomic ablation, operators may choose a period of watchful waiting before attempting a redo procedure.     

Left ventricular hypertrophy in chronically hypertensive ponies

Systemic arterial hypertension is associated with equine laminitis, a disease precipitated by gross over-ingestion of carbohydrates. We examined the hearts from nine chronically hypertensive (161 +/- 11/99 +/- 6 mmHg) laminitic ponies and nine normotensive (128 +/- 2/76 +/- 3 mmHg) ponies postmortem for signs of left ventricular hypertrophy. The hypertensive ponies had hearts which were significantly larger (7.77 +/- 0.26 g/kg bodyweight (BW) vs. 5.67 +/- 0.22 g/kg BW), as well as increased combined left ventricle and septum weight (4.99 +/- 0.21 g/kg BW vs. 3.67 +/- 0.20 g/kg BW) and left ventricular free wall weight (3.71 +/- 0.23 g/kg BW vs. 2.62 +/- 0.19 g/kg BW) (p less than 0.05). The right ventricular free wall weights were not significantly different. Mean left ventricular free wall thickness was increased significantly in the hypertensive ponies compared to the normotensive group (26.1 +/- 0.4 mm and 22.5 +/- 1 mm, respectively), but neither septal nor right ventricular free wall thickness was different. These findings demonstrate that left ventricular hypertrophy accompanies equine laminitis-induced hypertension.     

Idiopathic fascicular ventricular tachycardia

Idiopathic fascicular ventricular tachycardia is an important cardiac arrhythmia with specific electrocardiographic features and therapeutic options. It is characterized by relatively narrow QRS complex and right bundle branch block pattern. The QRS axis depends on which fascicle is involved in the re-entry. Left axis deviation is noted with left posterior fascicular tachycardia and right axis deviation with left anterior fascicular tachycardia. A left septal fascicular tachycardia with normal axis has also been described. Fascicular tachycardia is usually seen in individuals without structural heart disease. Response to verapamil is an important feature of fascicular tachycardia. Rare instances of termination with intravenous adenosine have also been noted. A presystolic or diastolic potential preceding the QRS, presumed to originate from the Purkinje fibers can be recorded during sinus rhythm and ventricular tachycardia in many patients with fascicular tachycardia. This potential (P potential) has been used as a guide to catheter ablation. Prompt recognition of fascicular tachycardia especially in the emergency department is very important. It is one of the eminently ablatable ventricular tachycardias. Primary ablation has been reported to have a higher success, lesser procedure time and fluoroscopy time.     

Mechanical behaviour of ventricular aneurysms

A mathematical model describes the mechanical behaviour of ventricular aneurysms assuming a spherical geometry for the left ventricle. Employing pressure-volume data obtained from normal dog hearts 1–2 hours after infarction, conditions are obtained on infarct thickness and angle of damage for ventricular rupture to occur. The results indicate that rupture is more likely to occur in the early period following infarction and that the dominant factor is the per cent thickness of the infarct.