确定性手术后的紫绀型先天性心脏病患者在极量运动过程中血浆容量的变化

Objectives: To evaluate changes in plasma volume(Δ PV)during exercise in patients with single ventricular physiology with cyanosis; post-Fontan patients; and in patients after right ventricular outflow tract reconstruction(RVOTR). Background: Compensatory mechanisms which regulate body fluid volumes operate in heart failure patients to maintain blood pressure. A better understanding of this pathophysiological process, especially during exercise, should help manage and follow such patients. Methods: Twenty-six CHD patients(14± 4 years), including 5 cyanotic patients, 12 after the Fontan operation, 9 after RVOTR, and 13 controls(14± 5 years), performed a treadmill exercise test. Δ PV from rest to peak was calculated and compared with changes in cardiovascular responses,plasma total protein(TP), norepinephrine(NE), osmolality(Osm), and blood lactate concentration(La). Results:Δ PV was smaller in CHD patients than in controls(Cyanotic:-5.9% , Fontan:-10.0% , RVOTR: -11.4% , Controls:-14.5% , p< 0.001). In all subjects, peak heart rate, systolic blood pressure and oxygen uptake correlated inversely with Δ PV(p< 0.05 to 0.005). Δ PV correlated inversely with changes in TP, NE, and La(p< 0.005 for all), but not with the change in Osm. In CHD patients, the Δ PV correlated only with the NE increase(p< 0.01). Conclusions: Δ PV is smaller in CHD patients than in controls, especially in cyanotic patients. The smaller increases in cardiovascular responses during exercise and La are associated with the small Δ PV. These mechanisms may help to maintain cardiac output and increased sympathetic nervous activity may be beneficial to ensure sufficient perfusion pressure against Δ PV during exercise.

先天性心脏病术后患者应用小剂量阿托品引起的负性变时效应与副交感神经介导的心血管反应有关

Objectives: To investigate the negative chronotropic response(NCR) to low-dose atropine in postoperative patients with congenital heart disease(CHD). Background: Low-dose atropine causes a NCR through the central nervous system muscarinic receptor and is attenuated in adult heart failure patients. It has never been evaluated in CHD patients. Methods: NCR corrected for basal heart rate(HR)(minimal HR/-basal HR=cNCR) was determined after low-dose atropine(3 μg/kg) administration in 124 postoperative CHD patients(97 biventricular repair and 27 Fontan patients) and 11 controls and was compared with the cardiac autonomic nervous and functional status. Results: The cNCR in simple CHD(post atrial or ventricular septal defect closure), complex biventricular CHD, and Fontan patients were 0.92±0.04, 0.94±0.04 and 0.96±0.04, respectively, and higher than in controls(0.87±0.03, p< 0.001). In the complex CHD patients, higher cNCR was mainly associated with the lower pharmacologically determined cardiac parasympathetic nervous tone(PST), HR variability, high atrial natriuretic peptide, and lower right ventricular ejection fraction(p< 0.0001). In Fontan patients, the lower βsensitivity of the sinus node and the PST mainly determined the higher cNCR(p< 0.01) and the cNCR did not correlate with either hemodynamics or exercise capacity. Conclusions: NCR is attenuated in proportion to the impaired cardiac parasympathetic nervous system and hemodynamics in postoperative complex biventricular CHD patients. In addition to PST, βsensitivity of the sinus node significantly influences the NCR in Fontan patients.

Fontan患者的功能状态与神经激素和心脏自主神经活动异常基本无关

Background-Impaired cardiac autonomic nervous activities and increased neurohumoral activities(CANA, NHA) characterize Fontan patients. However, the clinical significance of these changes is not clearly understood. Our purpose was to clarify the clinical significance of the CANA and NHA in stable Fontan patients. Methods and Results-We divided 22 atriopulmonary connection(APC) and 75 total cavopulmonary connection(TCPC) patients into 4 subgroups according to New York Heart Association (NYHA) class (1.8±0.6) and measured various CANA and NHA indices. All NHA indices were elevated in the symptomatic patients(P < 0.001).Natriuretic peptideswere higher in the APC than in the TCPC patients, and the hemodynamics showed no correlation with brain natriuretic peptide in the APC patients. Low arterial oxygen saturation and impaired hemodynamics greatly influenced all elevated NHA indices (P< 0.01), except for plasma renin activity, in the TCPC patients. Impaired CANA indices did not relate to NYHA class, although surgeries were associated with lower heart rate variability. In addition to poor correlation between NHA and CANA, age and ventricular morphology had no impact on all CANA and NHA indices, except for high norepinephrine in right ventricular Fontan patients. Conclusions-Although symptomatic Fontan patients exhibit higher NHA, CANA is not related to either NYHA class or NHA. APC itself is responsible for higher natriuretic peptides, and arterial oxygen desaturation has a great impact on elevated NHA in the TCPC patients. These characteristics of the NHA and CANA differ from those of heart failure patients with biventricular physiology.