Five dogs and two cats with a diagnosis of double-chambered right ventricle or primary infundibular stenosis were referred to undergo a combined cutting balloon and high-pressure balloon technique. At admission five cases were asymptomatic, one had a history of syncope and one had signs of right-sided congestive heart failure. Each patient underwent a complete transthoracic echocardiogram, thoracic radiographs, an angiogram and the combined interventional procedure. Median diameter of the right mid-ventricular stenosis was 4 mm (range 2-8.7 mm) in dogs, and it measured 1.9 and 2 mm in cats. Under general anesthesia initial dilation with an 8-mm × 2-cm cutting balloon was performed from a left external jugular vein approach followed by dilation with a high-pressure balloon (1.5:1 balloon diameter-right outflow tract diameter ratio). In one dog and the two cats the procedure was not completed due to technical issues. In the other four dogs the median intracavitary proximal chamber pressure decreased from 100 mmHg (range 70-150 mmHg) before the procedure to 57 mmHg (range 45-70 mmHg) post-dilation. Long-term follow-up (from six months to two years) showed complete or partial reverse remodeling of the proximal chamber with a median residual pressure gradient below 80 mmHg (range 46-75 mmHg) for all four dogs. This case series shows that this procedure should be considered in dogs with right ventricular outflow tract obstruction. In cats, the procedure might be feasible, if additional guidewire inventory were available.

Acute right ventricular pressure overload (RVPO) occurs following congenital heart surgery and often results in low cardiac output syndrome. We tested the hypothesis that the RV exhibits limited ability to modify substrate utilization in response to increasing energy requirements during acute RVPO after cardiopulmonary bypass (CPB). We assessed the RV fractional contributions (Fc) of substrates to the citric acid cycle in juvenile pigs exposed to acute RVPO by pulmonary artery banding (PAB) and CPB. Sixteen Yorkshire male pigs (median 38 days old, 12.2 kg of body weight) were randomized to SHAM (Ctrl, n = 5), 2-h CPB (CPB, n = 5) or CPB with PAB (PAB-CPB, n = 6). Carbon-13 (13 C)-labeled lactate, medium-chain, and mixed long-chain fatty acids (MCFA and LCFAs) were infused as metabolic tracers for energy substrates. After weaning from CPB, RV systolic pressure (RVSP) doubled baseline in PAB-CPB while piglets in CPB group maintained normal RVSP. Fc-LCFAs decreased significantly in order PAB-CPB > CPB > Ctrl groups by 13 C-NMR. Fc-lactate and Fc-MCFA were similar among the three groups. Intragroup analysis for PAB-CPB showed that the limited Fc-LCFAs appeared prominently in piglets exposed to high RVSP-to-left ventricular systolic pressure ratio and high RV rate-pressure product, an indicator of myocardial oxygen demand. Acute RVPO after CPB strongly inhibits LCFA oxidation without compensation by lactate oxidation, resulting in energy deficiency as determined by lower (phosphocreatine)/(adenosine triphosphate) in PAB-CPB. Adequate energy supply but also metabolic interventions may be required to circumvent these RV energy metabolic abnormalities during RVPO after CPB.

Background Right ventricular outflow tract (RVOT) stenosis after repair of tetralogy of Fallot has been linked with favorable right ventricular remodeling but adverse outcomes. The aim of our study was to assess the hemodynamic impact and prognostic relevance of right ventricular pressure load in this population. Methods and Results A total of 296 patients with repaired tetralogy of Fallot (mean age, 17.8±7.9 years) were included in a prospective cardiovascular magnetic resonance multicenter study. Myocardial strain was quantified by feature tracking technique at study entry. Follow-up, including the need for pulmonary valve replacement, was assessed. The combined end point consisted of ventricular tachycardia and cardiac death. A higher echocardiographic RVOT peak gradient was significantly associated with smaller right ventricular volumes and less pulmonary regurgitation, but lower biventricular longitudinal strain. During a follow-up of 10.1 (0.1-12.9) years, the primary end point was reached in 19 of 296 patients (cardiac death, n=6; sustained ventricular tachycardia, n=2; and nonsustained ventricular tachycardia, n=11). A higher RVOT gradient was associated with the combined outcome (hazard ratio [HR], 1.03; 95% CI, 1.00-1.06; P=0.026), and a cutoff gradient of ≥25 mm Hg was predictive for cardiovascular events (HR, 3.69; 95% CI, 1.47-9.27; P=0.005). In patients with pulmonary regurgitation ≥25%, a mild residual RVOT gradient (15-30 mm Hg) was not associated with a lower risk for pulmonary valve replacement. Conclusions Higher RVOT gradients were associated with less pulmonary regurgitation and smaller right ventricular dimensions but were related to reduced biventricular strain and emerged as univariate predictors of adverse events. Mild residual pressure gradients did not protect from pulmonary valve replacement. These results may have implications for the indication for RVOT reintervention in this population.

Background In complex congenital heart disease patients such as those with tetralogy of Fallot, the right ventricle (RV) is subject to pressure overload, leading to RV hypertrophy and eventually RV failure. The mechanisms that promote the transition from stable RV hypertrophy to RV failure are unknown. We evaluated the role of mitochondrial bioenergetics in the development of RV failure. Methods and Results We created a murine model of RV pressure overload by pulmonary artery banding and compared with sham-operated controls. Gene expression by RNA-sequencing, oxidative stress, mitochondrial respiration, dynamics, and structure were assessed in pressure overload-induced RV failure. RV failure was characterized by decreased expression of electron transport chain genes and mitochondrial antioxidant genes (aldehyde dehydrogenase 2 and superoxide dismutase 2) and increased expression of oxidant stress markers (heme oxygenase, 4-hydroxynonenal). The activities of all electron transport chain complexes decreased with RV hypertrophy and further with RV failure (oxidative phosphorylation: sham 552.3±43.07 versus RV hypertrophy 334.3±30.65 versus RV failure 165.4±36.72 pmol/(s×mL), P<0.0001). Mitochondrial fission protein DRP1 (dynamin 1-like) trended toward an increase, while MFF (mitochondrial fission factor) decreased and fusion protein OPA1 (mitochondrial dynamin like GTPase) decreased. In contrast, transcription of electron transport chain genes increased in the left ventricle of RV failure. Conclusions Pressure overload-induced RV failure is characterized by decreased transcription and activity of electron transport chain complexes and increased oxidative stress which are associated with decreased energy generation. An improved understanding of the complex processes of energy generation could aid in developing novel therapies to mitigate mitochondrial dysfunction and delay the onset of RV failure.

BACKGROUND: Acute pulmonary embolism (APE) patients with hypotension and/or shock should be evaluated for thrombolytic therapy, and hemodynamics often improves after thrombolytic therapy. Frontal plane QRS‑T (f[QRS-T]) angle, which is between the directions QRS axis and T axis, was described as a novel marker of ventricular repolarization heterogeneity. With right ventricular pressure overload, axis of heart may be affected and thrombolytic treatment may have an effect on this situation. This study aimed to investigate thrombolytic efficiency and effect on axis of heart by using f(QRS-T) angle.
METHODS: A total of 61 APE patients treated with thrombolytics and 71 APE patients treated without thrombolytics were included. Clinical findings and electrocardiogram (ECG) at diagnosis were collected. Second ECGs were included for patients with thrombolytics after 24 h, without thrombolytics after 72 h on average.
RESULTS: No significant differences were observed with regard to gender, age, hypertension, diabetes and cardiovascular disease. In patients with thrombolytics, respiratory rate, heart rate and pulmonary artery systolic pressure were significantly higher; oxygen saturation (Sat O2) as well as systolic and diastolic pressure were significantly lower. f(QRS-T) was markedly higher in APE with right ventricular pressure overload and changed significantly after thrombolytic therapy.
CONCLUSIONS: Right ventricular pressure overload in APE has an effect on f(QRS-T). In thrombolytic treatment, the change of f(QRS-T) angle may be a marker of successful thrombolysis.
UNASSIGNED: HINTERGRUND: Bei Patienten mit akuter Lungenembolie sowie Hypotonie und/oder Schock sollte eine Abwägung in Bezug auf eine thrombolytische Therapie erfolgen, oft verbessert sich die Hämodynamik nach thrombolytischer Behandlung. Der QRS-T-Winkel (f[QRS-T]) in der Frontalebene, der zwischen den Richtungen der QRS-Achse und der T‑Achse liegt, wurde als neuer Marker der Heterogenität bei der ventrikulären Repolarisation beschrieben. Bei rechtsventrikulärer Drucküberlastung kann die Herzachse betroffen sein, und auf diese Situation kann eine thrombolytische Therapie einen Effekt zeigen. Ziel der vorliegenden Studie war es, die Wirksamkeit einer thrombolytischen Behandlung und deren Auswirkungen auf die Herzachse unter Verwendung des Winkels f(QRS-T) zu untersuchen.
UNASSIGNED: In die Studie wurden 61 Patienten mit akuter Lungenembolie und Thrombolysetherapie sowie 71 Patienten mit akuter Lungenembolie ohne Thrombolysetherapie einbezogen. Dabei wurden die klinischen Befunde und das Elektrokardiogramm (EKG) bei Diagnosestellung ausgewertet. Ein zweites EKG wurde bei Patienten mit Thrombolyse nach 24 h, bei Patienten ohne Thrombolyse im Durchschnitt nach 72 h in die Auswertung einbezogen.
UNASSIGNED: Es fanden sich keine signifikanten Unterschiede in Bezug auf Geschlecht, Alter, Hypertonie, Diabetes mellitus und Herz-Kreislauf-Erkrankungen. Bei Patienten mit Thrombolyse waren die Atemfrequenz, Herzfrequenz und der pulmonalarterielle systolische Druck signifikant höher; die O2-Sättigung (Sat O2), der systolische und diastolische Druck waren dagegen signifikant niedriger. Der Winkel f(QRS-T) war bei Patienten mit akuter Lungenembolie und rechtsventrikulärer Drucküberlastung deutlich größer und änderte sich signifikant nach thrombolytischer Behandlung.
UNASSIGNED: Die rechtsventrikulärer Drucküberlastung bei akuter Lungenembolie wirkt sich auf f(QRS-T) aus. Bei thrombolytischer Therapie könnte die Änderung des Winkels f(QRS-T) ein Marker für die Ergebnisse nach erfolgreicher Thrombolyse sein.

Our aim was to describe the electrocardiographic features of critical COVID-19 patients.
We carried out a multicentric, cross-sectional, retrospective analysis of 431 consecutive COVID-19 patients hospitalized between 10 March and 14 April 2020 who died or were treated with invasive mechanical ventilation. This project is registered on ClinicalTrials.gov (identifier: NCT04367129). Standard ECG was recorded at hospital admission. ECG was abnormal in 93% of the patients. Atrial fibrillation/flutter was detected in 22% of the patients. ECG signs suggesting acute right ventricular pressure overload (RVPO) were detected in 30% of the patients. In particular, 43 (10%) patients had the S1Q3T3 pattern, 38 (9%) had incomplete right bundle branch block (RBBB), and 49 (11%) had complete RBBB. ECG signs of acute RVPO were not statistically different between patients with (n = 104) or without (n=327) invasive mechanical ventilation during ECG recording (36% vs. 28%, P = 0.10). Non-specific repolarization abnormalities and low QRS voltage in peripheral leads were present in 176 (41%) and 23 (5%), respectively. In four patients showing ST-segment elevation, acute myocardial infarction was confirmed with coronary angiography. No ST-T abnormalities suggestive of acute myocarditis were detected. In the subgroup of 110 patients where high-sensitivity troponin I was available, ECG features were not statistically different when stratified for above or below the 5 times upper reference limit value.
The ECG is abnormal in almost all critically ill COVID-19 patients and shows a large spectrum of abnormalities, with signs of acute RVPO in 30% of the patients. Rapid and simple identification of these cases with ECG at hospital admission can facilitate classification of the patients and provide pathophysiological insights.

OBJECTIVE: Right ventricular pressure overload, which can result in restrictive right ventricular physiology, predicts slow recovery after biventricular repair of congenital heart defects. The goal of the study was to assess how extubation in the operating room influences the postoperative course in these patients.
METHODS: Between January 2013 and June 2017, a total of 65 children [median age 0.96 (0.13-9.47) years; median weight 8 (3.05-25.8) kg] with right ventricular pressure overload underwent an intracardiac correction. The most common malformations were tetralogy of Fallot (n = 34) and double outlet right ventricle with pulmonary stenosis (n = 11). The patients were divided into 2 groups: the first (n = 36) comprised late extubated (LE) and the second (n = 29), early extubated (EE) children, immediately after chest closure in the operating room. Preoperative, perioperative and postoperative records were analysed retrospectively.
RESULTS: Children who had EE had a lower heart rate (EE 124.2 vs LE 133.6 bpm; P = 0.03), higher arterial blood pressure (systolic: EE 87.9 ± 9.35 vs LE 81.4 ± 12.0 mmHg; P = 0.029; diastolic: EE 51.1 ± 6.5 vs LE 45.9 ± 6.64 mmHg; P = 0.003), lower central venous pressure (EE 8.6 ± 1.89 mmHg vs LE 9.9 ± 2.42 mmHg; P = 0.03), fewer pleural effusions in the first 6 postoperative days (EE 1.38 ml/kg/day vs LE 5.98 ml/kg/day; P = 0.009), shorter time of dopamine support ≥3 μg/kg (EE 7.29 ± 12.26 h vs LE 34.78 ± 38.05 h, P < 0.001), shorter stays in the intensive care unit (EE 2.7 ± 2.67 vs LE 5.0 ± 4.77 days, P = 0.001) and hospital (EE 11.8 ± 4.79 vs LE 15.5 ± 7.8 days; P = 0.022).
CONCLUSIONS: Extubation in the operating room of children with right ventricular pressure overload undergoing biventricular correction is feasible and safe and has a beneficial effect on the postoperative course.

暂无摘要。

Surgical palliation or repair of complex congenital heart disease in early infancy can produce right ventricular (RV) pressure overload, often leading to acute hemodynamic decompensation. The mechanisms causing this acute RV dysfunction remain unclear. We tested the hypothesis that the immature right ventricle lacks the ability to modify substrate metabolism in order to meet increased energy demands induced by acute pressure overloading.
Twenty-two infant male mixed breed Yorkshire piglets were randomized to a sham operation (Control) or pulmonary artery banding yielding >2-fold elevation over baseline RV systolic pressure. We used carbon 13 (13C)-labeled substrates and proton nuclear magnetic resonance to assess RV energy metabolism. [Phosphocreatine]/[ATP] was significantly lower after pulmonary artery banding. [Phosphocreatine]/[ATP] inversely correlated with energy demand indexed by maximal sustained RV systolic pressure/left ventricular systolic pressure. Fractional contributions of fatty acids to citric acid cycle were significantly lower in the pulmonary artery banding group than in the Control group (medium-chain fatty acids; 14.5±1.6 versus 8.2±1.0%, long-chain fatty acids; 9.3±1.5 versus 5.1±1.1%). 13C-flux analysis showed that flux via pyruvate decarboxylation did not increase during RV pressure overloading.
Acute RV pressure overload yielded a decrease in [phosphocreatine]/[ATP] ratio, implying that ATP production did not balance the increasing ATP requirement. Relative fatty acids oxidation decreased without a reciprocal increase in pyruvate decarboxylation. The data imply that RV inability to adjust substrate oxidation contributes to energy imbalance, and potentially to contractile failure. The data suggest that interventions directed at increasing RV pyruvate decarboxylation flux could ameliorate contractile dysfunction associated with acute pressure overloading.

The rate of left ventricular pressure decrease during isovolumic relaxation is traditionally assessed algebraically via 2 empirical indices: the monoexponential and logistic time constants (τE and τL). Since the pattern of right ventricular (RV) pressure decrease is quite different from that of the left ventricular, we hypothesized that novel kinematic model parameters are more appropriate and useful to evaluate RV diastolic dysfunction.
Eight patients with pulmonary arterial hypertension (age 12.5±4.8 years) and 20 normal subjects (control group; age 12.3±4.4 years) were enrolled. The kinematic model was parametrized by stiffness/restoring Ek and damping/relaxation μ. The model predicts isovolumic relaxation pressure as a function of time as the solution of d2P/dt2+(1/μ)dP/dt+EkP=0, based on the theory that the pressure decay is determined by the interplay of inertial, stiffness/restoring, and damping/relaxation forces. In the assessment of RV diastolic function, τE and τL did not show significant differences between the pulmonary arterial hypertension and control groups (46.8±15.5 ms versus 32.5±14.6 ms, and 19.6±5.9 ms versus 14.5±7.2 ms, respectively). The pulmonary arterial hypertension group had a significantly higher Ek than the control group (915.9±84.2 s-2 versus 487.0±99.6 s-2, P<0.0001) and a significantly lower μ than the control group (16.5±4.3 ms versus 41.1±10.4 ms, P<0.0001). These results show that the RV has higher stiffness/elastic recoil and lower cross-bridge relaxation in pulmonary arterial hypertension.
The present findings indicate the feasibility and utility of kinematic model parameters for assessing RV diastolic function.