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Pathophysiology of impaired right and left ventricular function in chronic embolic pulmonary hypertension: changes after pulmonary thromboendarterectomy.

STUDY OBJECTIVES: This study sought to evaluate the pathophysiology of left and right heart failure in patients with chronic thromboembolic pulmonary hypertension (CTEPH) who were hospitalized to undergo pulmonary thromboendarterectomy (PTE). DESIGN: Thirty-nine patients (16 women and 23 men; mean +/- SD age, 55+/-12 years) with severe CTEPH were examined before and 13+/-8 days after PTE by way of transthoracic echocardiography and right heart catheterization. MEASUREMENTS AND RESULTS: Examination results confirmed in all cases that before surgery the right ventricles were enlarged and systolic function was impaired. Moderate to severe tricuspid valve regurgitation was observed. Left ventricular eccentricity indexes reflected a leftward displacement of the interventricular septum. End-diastolic left ventricular size and systolic function had decreased, and the left ventricular filling pattern showed impaired diastolic function. After surgery, mean pulmonary artery pressure was significantly lower (48+/- 10 mm Hg vs. 25+/-7 mm Hg; p<0.05). The calculated end-diastolic and end-systolic right ventricular areas had decreased: 30+/-7 cm(2) vs 21 +/-5 cm(2) (p<0.05) and 24+/-6 cm(2) vs. 14+/-4 cm(2) (p<0.05), respectively. Right ventricular fractional area change had increased (20+/-7% vs. 33+/-8%; p<0.05). Most of the patients exhibited a marked decrease in the severity of tricuspid regurgitation. Septal motion, left ventricular systolic function, and diastolic filling pattern returned to normal values (early to late diastolic left ventricular inflow ratio, 0.70+/-0.33 vs. 1.35+/-0.51; p<0.05). The mean cardiac index also improved (2.7+/-0.6 L/min/m(2) vs. 3.7+/-0.8 L/min/m(2)). CONCLUSIONS: In CTEPH, functions are impaired in the right as well as the left ventricles of the heart. Improved lung perfusion and the reduction of right ventricular pressure overload are direct results of PTE, which in turn bring a profound reduction of right ventricular size and a recovery of systolic function. Normalization of interventricular septal motion as well as improved venous return to the left atrium lead to a normalization of left ventricular diastolic and systolic function, and the cardiac index improves.

Adult↗

[A study of isolated tricuspid valve surgery late after left heart valve operation].

Management of severe tricuspid regurgitation late after left heart valve operation is controversial. There has been reluctance to the operation due to the high risk of repeat operation, coexistent right ventricular dysfunction and pulmonary hypertension. We investigated 6 cases of isolated tricuspid valve surgery (tricuspid valve replacement: 2, tricuspid valve plasty: 4) late after left heart valve operation. Before operation, these patients showed poor general condition (4 cases were NYHA III or IV) but good left ventricular function [mean ejection fraction (EF) 66 +/- 9.6%]. Hospital mortality was 0% and the mean mid-term actual event-free survival over 2 +/- 1.8 years was 80%. Most of patients demonstrated NYHA I and improvement of hepatomegaly after operation. There were many complications in 2 cases that had been performed previous operation more than 20 years before. In summary, the patient who complained symptoms due to right heart ventricular failure and showed good left ventricular function after left heart valve surgery should be considered to undergo tricuspid valve operation before the occurrence of other complications.

Aged↗

Stress-induced right ventricular ischemia in recurrent pulmonary outflow stenosis in repaired tetralogy of fallot.

Radionuclide uptake by the right ventricle during myocardial perfusion imaging is minimal compared with the left ventricular myocardium and is not given much importance. However, right ventricular hypertrophy from pressure or volume overload may increase right ventricular radiotracer uptake and demonstrate reversible stress-induced perfusion abnormalities in the presence of normal coronary arteries. We report a case of right ventricular ischemia secondary to right ventricular hypertrophy from recurrent right ventricular outflow tract stenosis in a patient with repaired tetralogy of Fallot. Advances in the management of congenital heart disease have led to more patients surviving to adulthood. These patients subsequently present to cardiologists in adulthood with sequelae or complications arising from previous surgery undertaken during childhood.

Adult↗

Haemodynamic evaluation of pulmonary hypertension.

Pulmonary hypertension is characterised by the chronic elevation of pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) leading to right ventricular enlargement and hypertrophy. Pulmonary hypertension may result from respiratory and cardiac diseases, the most severe forms occurring in thromboembolic and primary pulmonary hypertension. Pulmonary hypertension is most often defined as a mean PAP >25 mmHg at rest or >30 mmHg during exercise, the pressure being measured invasively with a pulmonary artery catheter. Doppler echocardiography allows serial, noninvasive follow-up of PAPs and right heart function. When the adaptive mechanisms of right ventricular dilatation and hypertrophy cannot compensate for the haemodynamic burden, right heart failure occurs and is associated with poor prognosis. The haemodynamic profile is the major determinant of prognosis. In both primary and secondary pulmonary hypertension, special attention must be paid to the assessment of pulmonary vascular resistance index (PVRI), right heart function and pulmonary vasodilatory reserve. Recent studies have stressed the prognostic values of exercise capacity (6-min walk test), right atrial pressure, stroke index and vasodilator challenge responses, as well as an interest in new imaging techniques and natriuretic peptide determinations. Overall, careful haemodynamic evaluation may optimise new diagnostic and therapeutic strategies in pulmonary hypertension.

Blood Pressure↗

Efficiency of prostacyclin in the treatment of protamine-mediated right ventricular failure and acute pulmonary hypertension.

Protamine is used after cardiopulmonary bypass was stopped in order to reverse the anticoagulant effects of heparin administered during open-heart operations. Adverse hemodynamic responses to protamine are common, ranging from minor perturbations to cardiovascular collapse. The aim of the present study was to investigate whether a prostacyclin is effective in the treatment of protamine-mediated acute pulmonary hypertension and right ventricular failure in the perioperative period of isolated coronary artery bypass grafting (CABG) operations. In sixty-eight (1.78%) of 3800 patients who underwent isolated CABG, acute pulmonary hypertension and right ventricular failure developed during or following the protamine infusion. These 68 patients were included in the study and were randomized into two groups. Thirty-eight of the patients received prostaglandin I(2) (PGI(2)), norepinephrine and dopamine (PGI(2) group), whereas 30 patients received nitroglycerin, norepinephrine and dopamine (control group). Hemodynamic data were recorded before and after the above drug combinations. The mean value of left ventricle ejection fraction significantly increased (p < 0.05) and mean values of central venous pressure, pulmonary artery systolic and diastolic pressure, pulmonary capillary wedge pressure and pulmonary vascular resistance significantly decreased (p < 0.05) in the PGI(2) group. The mean value of pulmonary capillary wedge pressure significantly decreased (p < 0.05) and the mean value of central venous pressure significantly increased (p < 0.05) in the control group. In conclusion, prostacyclin (PGI(2)) is effective in the treatment of protamine-mediated acute pulmonary hypertension and right ventricular failure in the perioperative period in isolated CABG operations. This finding may be an important contribution to the treatment of severe protamine complications during open-heart operations.

Acute Disease↗

Intraoperative assessment of right ventricular volume and function.

OBJECTIVE: Right ventricular function is an important aspect of global cardiac performance which affects patients' outcome after cardiac surgery. Due to its geometrical complexity, the assessment of right ventricular function is still a very difficult task. Aim of this study was to investigate the value of a new technique for intraoperative assessment of right ventricle based on transesophageal 3D-echocardiography, and to compare it to volumetric thermodilution by using a new generation of fast response thermistor pulmonary artery catheters. METHODS: Twenty-five patients with coronary artery disease underwent 68 intraoperative measurements by 3D-echocardiography and thermodilution simultaneously. Following parameters were analysed: right ventricular end-diastolic volume (RVEDV), end-systolic volume (RVESV) and ejection fraction (RVEF). Pulmonary, systemic and central venous pressures were simultaneously recorded. Segmentation of right ventricular volumes were obtained by the 'Coons-Patches' technique, which was implemented into the EchoAnalyzer, a multitask system developed at our institution for three-dimensional functional and structural measurements. RESULTS: Right ventricular volumes obtained by 3D-echocardiography did not show significant correlations to those obtained by thermodilution. Volumetric thermodilution systematically overestimates right ventricular volumes. Significant correlations were found between RVEF measured by 3D-echocardiography and those obtained by thermodilution (r=0. 93; y=0.2+0.80x; SEE=0.03; P<0.01). Bland-Altmann analysis showed that thermodilution systematically underestimates RVEF. The bias for measuring RVEF was +15.6% with a precision of +/-4.3%. The patients were divided into two groups according to left ventricular function. The group of patients with impaired function showed significantly lower right ventricular ejection fraction (44.1+/-4.6 vs. 55.1+/-3.9%; P<0.01). CONCLUSIONS: Three-dimensional echocardiography provides a useful non-invasive tool for intraoperative and serial assessment of right ventricular function. This new technique, which overcomes the limitations of previous methods, may offer key insights into management and outcome of patients with severe impairment of cardiac function.

Aged↗

[Severe right ventricular hypertension secondary to metastatic obstruction due to hepatocarcinoma].

Right ventricular hypertension (RVH) is an entity that could be expected in various cardiopulmonary diseases. Mechanical obstruction to the right ventricle outflow tract is a cause of RVH. We present the case of a 69 year-old male with a history of hepatocarcinoma previously treated. The developed RVH due to mechanical obstruction secondary to metastatic infiltration of the right ventricle. The clinical syndrome was characterized by systemic venous hypertension. Non-invasive studies, such as electrocardiogram and computed tomography scan limited the metastasis to the right ventricle; the diagnosis was confirmed by cardio-angiography and endocardial biopsy. The studies did not demonstrate neoplastic activity at any other level.

Aged↗

In the footsteps of senning: lessons learned from atrial repair of transposition of the great arteries.

The Senning operation has evolved from being the initial surgical correction that allowed survival in complete transposition of the great arteries to an integral part of the anatomic repair of congenitally corrected transposition. In patients with complete transposition, the Senning operation has given satisfactory initial and long-term surgical results, but the potential for right ventricular failure and atrial arrhythmias have drastically reduced its indications in the current era. The long-term follow-up and pertinent postoperative issues of the Senning operation will be reviewed, along with its newfound role in the anatomic repair of congenitally corrected transposition.

Arrhythmias, Cardiac↗

[In Process Citation]

In addition to ventricular arrhythmias, various forms of supraventricular arrhythmias (SVA) and atrioventricular (AV) and intraventricular (IV) conduction disturbances occur also in acute myocardial infarction (AMI). In the setting of AMI, SVA may be caused by relevant atrial ischemia or infarction. SVA complicate the course especially that of inferior, posterior and lateral AMI, SVA occur frequently also in the right ventricular myocardial infarction and in pericarditis. SVA appearing in the late phase of AMI are caused particularly by hemodynamic factors especially those of both left and right ventricular dysfunctions. Atrial dilatation and the increase of intraatrial pressure are also important factors in the genesis of SVA. The autonomous nervous system, electrolyte disturbances, acidosis and global hypoxia may operate as modulating factors in the development of SVA. AV conduction disturbances are significantly more frequent in patients with inferior than with anterior AMI. In inferior AMI, they are frequently caused by reflex parasympathetic activation. In the genesis of AV conduction disturbances, a significant role may be played also by the following mechanisms: Ischemia or necrosis of AV node or AV junction and the negative dromotropic effect of adenosine and potassium which are released to a great extent during myocardial ischemia and reperfusion. A high-degree AV block complicating the course of inferior AMI has a significantly better prognosis than that occurring in the setting of anterior AMI. In inferior AMI, AV block is frequently reversible, whereas in anterior AMI, it is persistent and irreversible. Early AV conduction disturbances, appearing within 24 hours of AMI have a better prognosis than those occurring in the late phase of AMI. Bundle branch blocks (BBB) complicating the course of AMI are caused by occlusion of bundle-related coronary artery or by serious ischemia in its bed. BBB is frequently a marker of a multivessel disease. New BBB appearing in AMI especially the right bundle branch block is considered as an predictor for the development of a complete AV block. Frequent and repetitive SVA as well as serious AV and IV conduction disturbances are frequently associated with a significantly worse clinically course of AMI and with increased mortality, with that of especially hospital mortality. However, this is usually not caused by SVA or AV and IV conduction disturbances per se. The major cause of death in these patients are heart failure cardiogenic shock and malignant ventricular arrthythmias due to larger AMI, significant reduction of left ventricular function and advanced coronary heart disease. Complex SVA as well as serious AV and IV conduction disturbances are usually considered as markers, but not as independent predictors for both increased hospital mortality and in some cases also for that of posthospital mortality. Their occurrence in AMI may help to identify the patients at great risk who require a very intensive treatment including aggressive management of extensive coronary heart disease. (Ref. 62.).

Journal Article↗

[Supraventricular arrhythmias and disorders of atrioventricular and intraventricular conduction in patients with acute myocardial infarct].

In addition to ventricular arrhythmias, various forms of supraventricular arrhythmias (SVA) and atrioventricular (AV) and intraventricular (IV) conduction disturbances occur also in acute myocardial infarction (AMI). In the setting of AMI, SVA may be caused by relevant atrial ischemia or infarction. SVA complicate the course especially that of inferior, posterior and lateral AMI. SVA occur frequently also in the right ventricular myocardial infarction and in pericarditis. SVA appearing in the late phase of AMI are caused particularly by hemodynamic factors especially those of both left and right ventricular dysfunctions. Atrial dilatation and the increase of intraatrial pressure are also important factors in the genesis of SVA. The autonomous nervous system, electrolyte disturbances, acidosis and global hypoxia may operate as modulating factors in the development of SVA. AV conduction disturbances are significantly more frequent in patients with inferior than with anterior AMI. In inferior AMI, they are frequently caused by reflex parasympathetic activation. In the genesis of AV conduction disturbances, a significant role may be played also by the following mechanisms: ischemia or necrosis of AV node or AV junction and the negative dromotropic effect of adenosine and potassium which are released to a great extent during myocardial ischemia and reperfusion. A high-degree AV block complicating the course of inferior AMI has a significantly better prognosis than that occurring in the setting of anterior AMI. In inferior AMI, AV block is frequently reversible, whereas in anterior AMI, it is persistent and irreversible. Early AV conduction disturbances, appearing within 24 hours of AMI have a better prognosis than those occurring in the late phase of AMI. Bundle branch blocks (BBB) complicating the course of AMI are caused by occlusion of bundle-related coronary artery or by serious ischemia in its bed. BBB is frequently a marker of a multivessel disease. New BBB appearing in AMI especially the right bundle branch block is considered as an predictor for the development of a complete AV block. Frequent and repetitive SVA as well as serious AV and IV conduction disturbances are frequently associated with a significantly worse clinical course of AMI and with increased mortality, with that of especially hospital mortality. However, this is usually not caused by SVA or AV and IV conduction disturbances per se. The major cause of death in these patients are heart failure, cardiogenic shock and malignant ventricular arrhythmias due to larger AMI, significant reduction of left ventricular function and advanced coronary heart disease. Complex SVA as well as serious AV and IV conduction disturbances are usually considered as markers, but not as independent predictors for both increased hospital mortality and in some cases also for that of posthospital mortality. Their occurrence in AMI may help to identify the patients at great risk who require a very intensive treatment including aggressive management of extensive coronary heart disease. (Ref. 62.)

Arrhythmias, Cardiac↗

Nitric oxide inhalation in acute pulmonary hypertension after cardiac surgery reduces oxygen concentration and improves mechanical ventilation but not mortality.

Impaired right-ventricular function may benefit from afterload reduction. Inhalation of nitric oxide (NO) reduces pulmonary hypertension without systemic circulatory depression. Influence of NO inhalation on oxygenation, ventilation, and hemodynamic parameters in 10 patients with acute pulmonary hypertension after cardiac surgery was examined in this study. Ten patients without NO treatment served as a control group. NO patients showed significantly improved oxygenation and recovery of right-ventricular function. Pulmonary artery pressure (12.8%), inspiratory oxygen demand (34.7%), PEEP (13.2%), and inspiration time (18.8%) decreased significantly during inhalation of nitric oxide. Mortality in both groups was identical. We therefore conclude that NO, by improving oxygenation and right-ventricular function, temporarily reduces invasiveness of mechanical ventilation. Reduction of invasiveness of ventilation did not influence mortality as compared with patients who did not receive NO. To finally estimate the benefit of NO inhalation, larger patient groups need to be examined.

Administration, Inhalation↗

Cardiac autonomic impairment and early myocardial damage involving the right ventricle are independent phenomena in Chagas' disease.

Cardiac autonomic impairment and right side heart failure are prominent features in patients with Chagas' disease, but no causal relationship between these phenomena has been disclosed and the pathophysiology of such manifestations is unclear. Aim of study was to assess the cardiac autonomic control and biventricular function in chagasic patients in early stages of the disease, using radionuclide angiography, Valsalva manoeuvre, head-up tilt and baroreflex sensitivity evaluation. Thirty-one chagasic patients with no clinical signs of Chagas' heart disease-16 in the indeterminate phase and 15 with sole organic digestive involvement-were studied, and results compared with those obtained in 14 normal volunteers. No significant differences were observed among the three groups, in regard to any systolic or diastolic parameter of LV function, including ejection fraction, peak ejection and filling rates and correspondent times, time to end-systole, and the standard deviation of phase values. The indeterminate and digestive groups of chagasics had significantly lower right ventricular ejection fraction (45.7 +/- 6.3 and 46.2 +/- 10.1 respectively) and peak ejection rate (respectively 2.8 +/- 0.6 and 2.9 +/- 0.6) and higher right ventricular phase standard deviation (22.4 +/- 5.9 and 20.1 +/- 5.6 degrees, respectively), as compared with the control group (53.6 +/- 4.3, 3.5 +/- 0.5, and 15.8 +/- 3.8 respectively for right ventricular ejection fraction, peak ejection rate and phase standard deviation). No significant differences were found between the results of autonomic evaluation in the control and indeterminate groups of chagasic patients. The group of digestive disease patients showed abnormally lower Valsalva ratio (1.5 +/- 0.15), baroreflex sensitivity (8.85 +/- 2.05 ms/mmHg) and parasympathetically-dependent heart rate response to tilt (8.85 +/- 8.42 beats/mm) and higher Valsalva delay (15.67 +/- 1.35 s) values, compared with the control group (respectively 1.85 +/- 0.49, 20.23 +/- 12.66 ms/mmHg, 21.61 +/- 5.77 beats/mm and 10.1 +/- 2.5 s). Thus, cardiac autonomic impairment is a prominent feature in chagasic patients with the digestive but not the indeterminate form of Chagas' disease. It bears no causative relationship to the early myocardial damage that is apparent only regarding right ventricular function, in both groups of patients. Early right ventricular dysfunction is a likely mechanism for the marked predominance of systemic over pulmonary congestion when heart failure supervenes in patients with Chagas' disease.

Adult↗

The usefulness of pulsed tissue Doppler for the clinical assessment of right ventricular function.

Standard Doppler echocardiographic evaluation of the right ventricular (RV) function has several limitations because of a difficult technical approach. The purpose of the present review was to investigate, even in the light of such problems, the usefulness of pulsed tissue Doppler (TD) during the assessment of RV transverse and longitudinal function on the basis of the regional velocities and time intervals. TD-derived (systolic and diastolic) velocities of the RV free wall and of the lateral tricuspid annulus have been used to establish reference values in healthy subjects and in different cardiac diseases. Some studies have shown the usefulness of myocardial systolic velocities for the detection of RV systolic failure at rest and of right coronary artery stenosis during stress. The myocardial early diastolic velocities, combined to Doppler standard tricuspid inflow measurements, represent reliable indexes of right chamber hemodynamics, the ratio between the Doppler tricuspid E velocity and the TD-derived early diastolic velocity of the lateral tricuspid annulus being positively related to the mean right atrial pressure after heart transplantation. Even the assessment of RV regional time intervals may have clinical implications. In particular, the relaxation time of the lateral tricuspid annulus, very short or even absent in healthy subjects increases progressively with the pulmonary systolic artery pressure and its length is strongly influenced also by the increasing RV wall thickness in septal hypertrophic cardiomyopathy and in hypertensive left ventricular hypertrophy. The interaction between the two ventricles is identified by assessing the TD velocities of the RV tricuspid annulus which are often associated with the corresponding velocities of the mitral annulus in different pathologies. On the grounds of these studies, the clinical use of pulsed TD merits consideration. Longitudinal follow-up of TD RV patterns will be useful to evaluate the progression from early RV wall dysfunction until the development of global RV failure and the possible beneficial effect of cardiac drugs on RV function as determined by TD evaluation.

Cardiomyopathy, Hypertrophic↗

Implantable cardioverter/defibrillator therapy in arrhythmogenic right ventricular cardiomyopathy: single-center experience of long-term follow-up and complications in 60 patients.

BACKGROUND: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a major cause of ventricular tachycardia (VT) and cardiac arrest in young patients. We hypothesized that treatment with implantable cardioverter/defibrillators (ICDs) is safe and improves the long-term prognosis of ARVC patients at high risk of sudden death. METHODS AND RESULTS: Sixty patients with ARVC (aged 43+/-16 years) were treated with transvenous ICD systems. Despite a higher number of right ventricular sites tested for adequate lead positions (P<0.05), lower R-wave amplitudes (P<0.001) were achieved in ARVC patients compared with other entities. During follow-up of 80+/-43 months (396 patient-years), event-free survival was 49%, 30%, 26%, and 26% for appropriate ICD therapies and 79%, 64%, 59%, and 56% for potentially fatal VT (>240 bpm) after 1, 3, 5, and 7 years, respectively. Multivariate analysis identified extensive right ventricular dysfunction as an independent predictor of appropriate ICD discharge. Fifty-three adverse events occurred in 37 patients during the perioperative (n=10) or follow-up (n=43) period, mainly related to the leads (n=31 in 21 patients). No lead perforation was observed. Freedom from adverse events was 90%, 78%, 56%, and 42% and freedom from lead-related complications was 95%, 85%, 74%, and 63% after 1, 3, 5, and 7 years, respectively. CONCLUSIONS: These results strongly suggest an improvement in long-term prognosis by ICD therapy in high-risk patients with ARVC. However, meticulous placement and long-term observation of transvenous lead performance with focus on sensing function are required for the prevention and/or early recognition of disease progression and lead-related morbidity during long-term follow-up of ICD therapy in ARVC.

Adolescent↗

Quantitative angiographic analysis of right ventricular global function in normal incidences and in patients with coronary artery disease.

At present right ventriculography data cannot be accurately estimated owing to the absence of software for quantitative analysis of the right ventricle (RV) volumes and function. The aim of this study was to use existing software for left ventriculography analysis to estimate right ventricular volumes and function in patients without coronary lesions and in those with coronary artery disease (CAD). Thirty-two patients without significant lesions of coronary arteries and 20 patients with CAD were examined with left ventriculography and right atriography. Each examination was performed in 2 projections: 30 degrees right anterior oblique (RAO 30 degrees) and 60 degrees left anterior oblique (LAO 60 degrees) projections. Correction factor (CF) was obtained by finding the ratio between stroke volumes of the left and right ventricles. The mean CF was 0.9243+/-0.2887 for patients without CAD and 0.8758+/-0.2232 for patients with CAD. Such calculation is the easiest and quite accurate method of determining RV volumes and function by using existing software of quantitative angiographic analysis.

Adult↗

Optical mapping of ventricular defibrillation in isolated swine right ventricles: demonstration of a postshock isoelectric window after near-threshold defibrillation shocks.

BACKGROUND: Investigators who studied ventricular defibrillation by use of optical mapping techniques failed to observe an initial defibrillation event (isoelectric window or quiescent period) shown by electrode mapping studies. This discrepancy has important implications for the mechanisms of defibrillation. The purpose of the present study was to demonstrate an optical equivalent of an isoelectric window after a near-threshold defibrillation shock. Methods and Results-- We studied 10 isolated, perfused swine right ventricles. Upper limit of vulnerability was determined by shocks on T waves. A 50% probability of successful defibrillation (DFT50) was determined with an up-down algorithm. Immediately after unsuccessful defibrillation shock, new wavefronts were generated. When the shock strength was low, immediate reinitiation of reentry and ventricular fibrillation might occur without a postshock isoelectric window. However, if the shock strength was within 50 V of DFT50 (near-threshold), a synchronized activation occurred, followed by organized repolarization that ended 64+/-18 ms after shock. After a period of quiescence (18+/-24 ms), activation recurred 83+/-33 ms after shock and reinitiated ventricular fibrillation. Similar patterns of activation, including a quiescent period, were observed after shock was applied on the T wave of the paced beat that induced ventricular fibrillation. Upper limit of vulnerability correlated well with DFT50. CONCLUSIONS: In isolated swine right ventricles, an optical equivalent of an isoelectric window exists after near-threshold defibrillation shocks. These findings support the idea that a near-threshold defibrillation shock terminates all activation wavefronts but fails to halt ventricular fibrillation because the same shock reinitiates ventricular fibrillation after an isoelectric window.

Action Potentials↗

Differential right and left ventricular diastolic tolerance to acute afterload and NCX gene expression in Wistar rats.

This study evaluated right ventricular (RV) and left ventricular (LV) diastolic tolerance to afterload and SERCA2a, phospholamban and sodium-calcium exchanger (NCX) gene expression in Wistar rats. Time constant tau and end diastolic pressure-dimension relation (EDPDR) were analyzed in response to progressive RV or LV afterload elevations, induced by beat-to-beat pulmonary trunk or aortic root constrictions, respectively. Afterload elevations decreased LV- tau, but increased RV-tau. Whereas LV- tau analyzed the major course of pressure fall, RV- tau only assessed the last fourth. Furthermore, RV afterload elevations progressively upward shifted RV EDPDR, whilst LV afterload elevations did not change LV-EDPDR. SERCA2a and phospholamban mRNA were similar in both ventricles. NCX-mRNA was almost 50 % lower in RV than in LV. Left ventricular afterload elevations, therefore, accelerated the pressure fall and did not induce diastolic dysfunction, indicating high LV diastolic tolerance to afterload. On the contrary, RV afterload elevations decelerated the late RV pressure fall and induced diastolic dysfunction, indicating small RV diastolic tolerance to afterload. These results support previous findings relating NCX with late Ca(2+) reuptake, late relaxation and diastolic dysfunction.

Animals↗