Mechanism of overshoot in cardiac function during recovery from submaximal exercise in man.

BACKGROUND: A sudden increase (overshoot) in the left ventricular ejection fraction during the recovery from maximal exercise has been reported in patients with coronary artery disease, but its mechanism has not been fully clarified. We investigated whether this phenomenon may occur in normal subjects, and whether it depends on the intensity of exercise. METHODS: Thirteen normal subjects (mean [+/- SD] age, 59 +/- 8 years old) performed two levels (25 W and 50 W) of mild-intensity, constant-work-rate exercise for 6 min on a cycle ergometer. Left ventricular function was monitored continuously during the recovery from exercise using a computerized cadmium telluride detector. RESULTS: An overshoot was observed in the ejection fraction during the first minute of recovery compared with the end-exercise value. The overshoot in the ejection fraction during recovery after the 50-W exercise was greater than that seen after the 25-W exercise. An overshoot phenomenon in stroke volume was also observed during the recovery from 50-W exercise. CONCLUSIONS: The overshoot in cardiac function observed during the early phase of recovery, which was caused mainly by an immediate decrease in end-systolic volume, occurred even after exercise of mild intensity. This phenomenon appears to suggest the existence of a transient mismatch between cardiac contractility and afterload reduction during the recovery from mild-intensity exercise, even in normal subjects.     

Beat-to-beat evaluation of cardiac function during recovery from upright bicycle exercise in patients with coronary artery disease

The purpose of this study was to evaluate the time course of cardiac function during recovery from upright bicycle exercise in patients with coronary artery disease. Twelve patients with coronary artery disease performed a symptom-limited exercise test on a cycle ergometer. Left ventricular function was continuously monitored during exercise and recovery with a computerized cadmium telluride detector following the intravenous injection of technetium-labeled red blood cells. Although the end-diastolic volume (153.4 +/- 76.1 ml) and end-systolic volume (100.5 +/- 67.3 ml) at the end of exercise were significantly higher than the respective resting values, stroke volume (52.8 +/- 16.1 ml) and ejection fraction (38.0 +/- 12.2%) were not different from the respective resting values. The recovery of cardiac output was relatively slow compared with that of heart rate, because stroke volume rose sharply early in recovery. The rise in stroke volume was chiefly a result of a significant decrease in end-systolic volume between 1 and 4 minutes of recovery. These changes may result from an immediate afterload reduction coupled with a relatively slow decrease in sympathetic stimulation. The time course of cardiac function during recovery from exercise in cardiac patients is substantially different from that of normal subjects and may be a sensitive way to evaluate the peripheral vascular function and deteriorated cardiac function in cardiac patients.     

Hemoglobin function in stored blood

Summary Inorganic phosphate which is known to stimulate red cell glycolysis is present in one of the preservatives for storing whole blood, citrate-phosphate-dextrose (CPD), but not the other, acid-citrate-dextrose (ACD). Both of these preservatives for liquid storage were developed before 2,3-diphosphoglycerate (2,3-DPG) was found to be necessary for normal hemoglobin function. In a recent study we have shown that very high concentrations of phosphate (10, 15, and 20 mM) were deleterious for maintaining 2,3-DPG. In the present study a lower range of phosphate concentrations (2, 4, 6, and 8 mM) was studied for maintenance of 2,3-DPG and ATP during storage under blood banking conditions. The lowest concentration, 2 mM, which corresponds to CPD was found to be the best concentration for maintaining 2,3-DPG and thus hemoglobin function. Four mM phosphate was not quite as good but better than no phosphate. Six and 8 mM phosphate were considerably worse.

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Zusammenfassung Im Anschluß an vorangegangene Arbeiten wurde die Anwendung von geringen Phosphatmengen (2–8 mM) zur Stabilisierung von 2,3-DPG und ATP während der Lagerung von Blut unter Blutbankbedingungen geprüft, um die Hämoglobinfunktion aufrecht zu erhalten. Am besten bewährte sich die 2mM-Konzentration des anorganischen Phosphats, während die 4mM-Konzentration weniger wirkungsvoll war. 6–8 mM-Konzentrationen wurden als ungeeignet befunden, die Stabilisierung von 2,3-DPG und ATP zu gewährleisten.

     

Altered cardiac autonomic function after recovery from COVID‐19

BackgroundAutonomic dysfunction may occur during the acute phase of COVID‐19. Heart rate variability (HRV) is a useful tool for the assessment of cardiac sympathetic and parasympathetic balance. We aimed to evaluate cardiac autonomic function by using HRV in subjects after recovery from COVID‐19 who had previously symptomatic and were followed outpatiently.MethodsThe study group composed of 50 subjects with a confirmed history of COVID‐19 and the control group composed of 50 healthy subjects without a history of COVID‐19 and vaccination. All the study participants underwent 2‐dimensional, pulsed‐ and tissue‐Doppler echocardiographic examinations and 24‐hour Holter monitoring for HRV analysis.ResultsTime domain parameters of SDNN, SDANN, SDNNi, RMSSD, pNN50, and HRV triangular index were all decreased in the study group when compared with the control group. Frequency domain parameters of TP, VLF, LF, HF, and HFnu were also decreased in the study group in comparison with the control group. LFnu was similar between groups. Nonlinear parameters of HRV including α₁ and α₂ decreased in the study group. By contrast, Lmax, Lmean, DET, REC, and Shannon entropy increased in the study population. Approximate and sample entropies also enhanced in the study group.ConclusionsThe present study showed that all three domain HRV significantly altered in patients after recovery from COVID‐19 indicating some degree of dysfunction in cardiac autonomic nervous system. HRV may be a useful tool for the detection of preclinical autonomic dysfunction in this group of patients.     

慢性心力衰竭患者心功能恢复的相关因素研究

目的:分析影响慢性心力衰竭(CHF)患者心功能恢复的相关因素。方法:连续入选232例诊断为CHF并至少随访1年的患者,记录患者临床和生化资料,并定期行超声心动图检测。Logistic回归分析评估影响CHF患者心功能恢复的相关因素。结果:232例患者中56例患者心功能恢复,176例患者心功能未恢复。扩张型心肌病患者较缺血性心肌病患者心功能更易恢复(P0.05),围生期心肌病患者预后良好。与体质量正常或过轻患者相比,体质量指数(BMI)较高的CHF患者心功能更易恢复(P0.05)。心功能恢复患者基础心率偏快,β受体阻滞剂耐受剂量较大,药物治疗后心率下降较明显(P均0.001)。Logistic回归分析显示,患者心功能恢复与CHF病因(OR=1.322,95%CI:1.256~1.392,P=0.04)和β受体阻滞剂剂量(OR=2.483,95%CI:2.359~2.614,P0.001)相关。结论:CHF病因和β受体阻滞剂剂量与CHF患者心功能恢复相关,BMI及基础心率较高患者心功能易于恢复。     

Effects on recovery during acidosis in cardiac myocytes overexpressing CaMKII

Recovery of intracellular Ca transients and fractional shortening during late phase acidosis are suggested to be associated with CaMKII-dependent processes of which phospholamban (PLB) phosphorylation may play an important role. To test whether increased expression levels of CaMKII may further enhance recovery, we investigated myocytes from CaMKIIdelta(C) transgenic (TG) mice (cytosolic localized CaMKII) having heart failure vs. wild-type littermates (WT). Furthermore, mouse and rabbit myocytes overexpressing CaMKIIdelta(C) using adenovirus-mediated gene transfer (vs. LacZ control) were investigated. Fractional shortening (% vs. resting cell length, % RCL) was assessed during control conditions (pH 7.4) and during acidosis (pH 6.5). Ca transients were measured using fluo-3 (DeltaF/F(0), 10 microM). In WT mouse myocytes, fractional shortening clearly recovered by 90% from 4.6+/-0.6 to 7.2+/-0.7% RCL during late acidosis. In parallel, Ca transients increased from 2.01+/-0.11 to 2.33+/-0.15 DeltaF/F(0). When blocking CaMKII (KN-93, 1 microM), recovery of Ca transients and shortening could be completely abolished. In contrast, in CaMKIIdelta(C) TG mouse myocytes shortening recovered only by 32% from 3.4+/-0.6 to 4.4+/-0.5% RCL (P<0.05 vs. WT using ANOVA). In parallel, Ca transients increased only slightly from 1.75+/-0.15 to 1.84+/-0.13 DeltaF/F(0) (P<0.05 vs. WT using ANOVA). In accordance, SR Ca content (measured by caffeine contractures, 10 mM) in WT significantly increased during late acidosis but not in CaMKIIdelta(C) TG mice. In contrast, in mouse and rabbit myocytes overexpressing CaMKIIdelta(C) by means of adenovirus-mediated gene transfer, recovery of fractional shortening and Ca transients was not impaired during late acidosis but even slightly improved vs. LacZ control (P<0.05 vs. CaMKIIdelta(C) using ANOVA for mouse and rabbit myocytes). This was associated with significantly increased SR Ca content during late acidosis in CaMKIIdelta(C) as compared to LacZ. CaMKII-dependent PLB Thr-17 phosphorylation, contributing to increased SR Ca uptake, was significantly increased in CaMKIIdelta(C) transfected rabbit myocytes vs. LacZ in the light of unchanged SR Ca ATPase and PLB protein expression. CaMKII inhibition completely prevented recovery of all parameters in both CaMKIIdelta(C) and LacZ. In summary and in contrast to our initial hypothesis, we showed for the first time that TG CaMKIIdelta(C) overexpression (i.e., chronic overexpression) in mice with heart failure clearly resulted in impaired recovery associated with impaired SR Ca loading during late acidosis vs. WT. This may be due to decreased SR Ca ATPase and PLB expression as reported previously. In contrast, adenovirus-mediated gene transfer of CaMKIIdelta(C) in mouse and rabbit myocytes (i.e., acute overexpression) did not result in impaired but even slightly improved recovery associated with increased SR Ca load during late acidosis as compared to LacZ. This most likely was due to higher PLB Thr-17 phosphorylation in CaMKIIdelta(C) myocytes. In conclusion, possible beneficial effects by therapeutical CaMKIIdelta(C) stimulation on the ability to recover from acidosis may be challenged by altered expression levels of its target proteins and should be carefully considered.     

Contact-force recovery predicts the absence of cardiac perforation during steam pops

Journal of Interventional Cardiac Electrophysiology - Cardiac perforation (CP) is an uncommon but clinically important complication of radiofrequency ablation (RFA). We previously showed that...     

Glucose-insulin infusion improves cardiac function during fetal tachycardia

OBJECTIVES: The aim of this work was to study the effects of substrate deficiency and supplementation on cardiac function during fetal tachycardia. BACKGROUND: Although sustained fetal tachycardia may lead to cardiac failure and intrauterine death, neonatal tachycardia is generally better tolerated. Fetal myocardial energy production relies almost solely on glucose as substrate. We hypothesized that increased substrate availability by glucose-insulin (GI) infusion would improve fetal myocardial responses to tachycardia. METHODS: We used three porcine models: 1) an isolated fetal heart model; 2) an in vivo fetal model; and 3) an in vivo closed-chest neonatal model. Each animal was randomized to control or GI treatment during tachycardia. In model 1, the controls were perfused with conventional Krebs-Henseleit solution containing a glucose concentration of 5.5 mmol/l; the GI hearts received double glucose concentration and added insulin. In models 2 and 3, the GI animals received insulin in a 20% glucose solution. All hearts were exposed to 90 min of pacing at 250 to 330 beats/min. RESULTS: The isolated fetal hearts in the GI group showed no decline in dP/dt(max) during pacing, while the controls declined. In the in vivo fetal hearts, dP/dt(max) remained unchanged in the GI group and decreased significantly in the control group. Myocardial glycogen content was higher in the GI group than in controls. Functional indexes remained unchanged among both neonatal groups despite a higher glycogen content in the GI group. CONCLUSIONS: Glucose-insulin infusion during fetal tachycardia has a beneficial effect on myocardial metabolism and cardiac function. These observations may have direct clinical relevance to the management of fetal arrhythmia.     

间歇有氧运动训练改善肥胖小鼠缺血后心脏功能恢复

目的 探讨有氧间歇运动训练（AIT）对高脂饮食诱导的肥胖小鼠心肌缺血再灌注（MI/R）损伤的影响和相关机制。 方法 30只2月龄C57小鼠随机分为:正常对照组;高脂饮食组;高脂饮食间歇训练组。喂养12周后,建立急性MI/R模型（缺血30 min,再灌注4 h）。于再灌注结束后不同时间点采用超声心动仪检测心脏功能,Western blot法检测心脏相关信号表达。 结果 与正常对照组相比,12周高脂饮食喂养导致小鼠肥胖,体质量显著增加（P<0.05）;AIT可有效降低高脂饮食肥胖小鼠的体质量,增加心脏质量/胫骨长度比率（P<0.05）;与正常对照组相比,高脂饮食肥胖小鼠MI/R损伤显著加重（P<0.05）;AIT可有效减轻肥胖小鼠心肌损伤,减小心肌梗死面积和血清LDH水平（均P<0.05）;AIT还显著改善MI/R后心肌功能恢复,有效提高左室射血分数（EF）和左室短轴缩短率（FS）（均P<0.05）。与高脂饮食组相比,AIT可显著增强高脂饮食肥胖小鼠心肌线粒体SIRT3和MnSOD表达,减少高脂饮食组MI/R心肌组织氧化应激（均P<0.05）。 结论 AIT可有效提高高脂饮食肥胖小鼠心肌线粒体SIRT3和MnSOD表达,增加线粒体抗氧化酶活性,进而减轻肥胖小鼠的MI/R损伤,促进缺血后心脏功能恢复。     

Ambulatory ventricular function monitoring for serial assessments of cardiac function during exercise

An ambulatory ventricular function monitor (VEST) facilitated measuring left ventricular (LV) function, and performing electrocardiography (ECG) in a natural environment. To assess cardiac response to a variety of exercises, LV function was serially recorded for each of 18 normal subjects using a VEST. The VEST detector was fixed over the LV region following the gated blood pool scan, and the beat-to-beat LV time-activity curve and ECG were continuously recorded. After a baseline recording was made with the subject sitting quietly, the subject performed on a bicycle exercise (n = 16), on a treadmill (n = 14), and by walking up 10-16 flights of stairs (n = 18) while wearing the VEST. The beat-to-beat radionuclide data were averaged for 15-30 seconds to calculate ejection fraction (EF), relative end-diastolic (EDV) and end-systolic (ESV) volumes, and the heart rate. Serial LV function monitoring during each exercise, particularly while walking upstairs and on a treadmill, documented rapid increases in EF during the early stages of exercise, with increases in EDV, decreases in ESV, and no change in EF in the later stages. Heart rate and systolic blood pressure increased progressively with successive stages. The pressure rate product at the peak exercise was highest during treadmill exercise (32,600) and lowest while climbing stairs (24,700). Immediately after exercise, EDV and ESV rapidly decreased and EF increased further, particularly after bicycle and treadmill exercise. These data demonstrate that the VEST can measure LV function continuously in an ambulatory environment, and that it is an effective means of evaluating normal cardiac physiology during various exercises.     

Overshoot phenomena of respiratory gas variables during exercise recovery in cardiac patients

BACKGROUND: Transient increases (overshoot) in respiratory gas variables have been observed during exercise recovery, but their clinical significance is not clearly understood. Our group evaluated the relationship between the presence of overshoot of respiratory gas variables and the parameters obtained from cardiopulmonary exercise testing (CPX). Methods and Results: In total, 227 patients with various cardiac diseases underwent CPX. The overshoot phenomena of O? uptake (·VO?), ·VO?/heart rate (O?-pulse), and CO? output (·VCO?) were analyzed by respiratory gas analysis during recovery after maximal exercise. The overshoot of ·VO?, O?-pulse, and ·VCO? were recognized in 11 (5%), 43 (19%), and 12 (5%) patients, respectively. Compared with the patients without a ·VO? overshoot, those with a ·VO? overshoot had a significantly lower peak ·VO? (12.3±3.7 vs. 17.9±6.2ml·min?1·kg?1, P=0.003), lower anaerobic threshold (9.4±1.7 vs. 12.4±3.3 ml·min?1·kg?1, P=0.001), higher ·VE-·VCO? slope (38.0±5.2 vs. 33.2±9.6, P=0.013), and lower left ventricular ejection fraction (LVEF) (39.9±22.8 vs. 55.8±16.8%, P=0.003). Similar findings were obtained for the patients with an O?-pulse overshoot and those with a ·VCO? overshoot. CONCLUSIONS: The overshoot phenomena of respiratory gas variables during recovery after maximal exercise are correlated with impaired cardiopulmonary function during exercise in cardiac patients.     

Hemoglobin A1c predicts heart failure hospitalization independent of baseline cardiac function or B-type natriuretic peptide level

Aims

Diabetes is a major risk factor for heart failure (HF). We examined whether baseline HbA_1c level predicts HF incidence independent of other HF risk factors, including baseline cardiac structural and functional abnormalities.

Methods

In patients with type 2 diabetes, multivariable Cox regression models were constructed to examine the independent association between baseline HbA_1c and future HF hospitalization.

Results

In 608 subjects (mean age, 66.5 years; men, 68%; mean HbA_1c, 9.1% (76 mmol/mol)), 92 were hospitalized for HF during a median follow-up of 6 years. For a 1% (11 mmol/mol) increase in baseline HbA_1c, the hazard ratio for HF was 1.23 (95% confidence interval, 1.1–1.7, p < 0.001) with adjustment for age, sex, body mass index, blood pressure and plasma B-type natriuretic peptide (BNP) level. The effect of HbA_1c on HF was independent of baseline left ventricular (LV) ejection fraction, the ratio of peak early to late diastolic filling velocity, and prevalent/incident coronary heart disease (CHD), and was more evident in patients with enlarged LV, decreased systolic function, prevalent CHD, or prevalent HF.

Conclusion

In patients with type 2 diabetes, HbA_1c significantly predicts future HF hospitalization independent of baseline BNP level or echocardiographic parameters.     

Atrial function during cardiac arrest caused by ventricular fibrillation

OBJECTIVES: To report observations on preserved regular atrial electrical and mechanical systole during ventricular fibrillation (VF) and to quantitate blood flow generated by atrial contractions in this setting. METHODS: In 10 rats, right atrial pressure pulses were continuously recorded before and for an interval of 8 min after inducing VF. In 3 isolated, perfused rat hearts, epicardial right atrial electrograms were recorded after inducing VF. In 15 pigs, transesophageal echo-Doppler measurements were obtained with pulsed and color-Doppler visualization of flow across the mitral valve after onset of VF. RESULTS: In each rat, regular right atrial pressure pulses were documented during VF. These persisted over an average interval of 7.5 min. In isolated, perfused hearts, right atrial contractions were accompanied by regular atrial depolarizations. In pigs, regular atrial contractions generated atrial stroke volumes of approximately 12 mL, or 25% of prearrest values during the first minute after onset of VF, but those declined to approximately 6 mL after 10 min of untreated cardiac arrest. Blood flow from the left atrium into the left ventricle failed to advance significantly into the systemic circuit. During atrial diastole, we observed reversal of flow into the left atrium. CONCLUSIONS: Atrial contractions are preserved during the initial 8 min or more after cardiac arrest due to VF. Substantial forward flow into the left ventricle failed to advance through the outflow tract but regurgitated into the atrium during atrial diastole.     

Exocrine pancreatic function during the early recovery phase of acute pancreatitis

BACKGROUND:Exocrine pancreatic dysfunction has been reported in humans in the convalescent period after acute pancreatitis,but the data are scarce and conflicting.This study aimed to prospectively assess the exocrine pancreatic function in patients with acute pancreatitis at the time of their refeeding. METHODS:Fecal elastase-1 was determined on the day of refeeding in all consecutive acute pancreatitis patients with their first episode of the disease.They were 75 patients including 60(80.0%)patients with m...