R. Puranik

Resistance training improves cardiac output, exercise capacity and tolerance to positive airway pressure in Fontan physiology☆

BACKGROUND Subjects with Fontan-type circulation have no sub-pulmonary ventricle and thus depend exquisitely on the respiratory bellows and peripheral muscle pump for cardiac filling. We hypothesised that resistance training to augment the peripheral muscle pump might improve cardiac filling, reduce inspiratory-dependence of IVC return to the heart and thus improve exercise capacity and cardiac output on constant positive airway pressure (CPAP). METHODS Eleven Fontan subjects (32+/-2 years, mean+/-SEM) had cardiac magnetic resonance imaging (MRI) and exercise testing (CPET); six underwent 20 weeks of high-intensity resistance training; others were non-exercising controls. After training, CPET was repeated. Four trainers had MRI with real-time flow measurement at rest, exercise and on CPAP in the trained state and following a 12-month detrain. RESULTS In the trained state, muscle strength increased by 43% (p=0.002), as did total muscle mass (by 1.94 kg, p=0.003) and peak VO2 (by 183 ml/min, p=0.02). After detraining, calf muscle mass and peak workload had fallen significantly (p<0.03 for both) as did peak VO2 (2.72 vs. 2.18 l/min, p<0.001) and oxygen pulse, a surrogate for SV (16% lower, p=0.005). Furthermore after detraining, SV on MRI decreased at rest (by 11 ml, p=0.01) and during moderate-intensity exercise (by 16 ml, p=0.04); inspiratory-dependent IVC blood return during exercise was 40% higher (p=0.02). On CPAP, cardiac output was lower in the detrained state (101 vs. 77 ml/s, p=0.03). CONCLUSIONS Resistance muscle training improves muscle mass, strength and is associated with improved cardiac filling, stroke volume, exercise capacity and cardiac output on CPAP, in adults with Fontan-type circulation.

Presence Of Left Ventricular Non Compaction In Hypertrophic Cardiomyopathy Is Associated With Arrhythmia

Results 66% of the patients were male, mean age 52 ± 18 years, mean wall thickness was 19 ± 4 mm. Amongst the 9 patients with LVNC, 5 had VT/VF, 2 had SVT and 2 had syncope. Patients with LVNC had a significantly higher prevalence of ventricular arrhythmia than those without LVNC (56% vs 18%, p = 0.03), with a relative risk of 3.0 (95% CI 1.3 6.9). LV septal thickness (18.4 ± 5.6 mm vs 18.7 ± 3.5 mm, p = 0.9) and ejection fraction (70 ± 7.7 vs 70 ± 10.5%, p = 0.9) did not significantly differ between those with LVNC and those without. Presence of LV scar assessed by late gadolinium enhancement was similar between the groups (89% vs 73%, p = 0.7). Conclusions Presence of LVNC may be associated with ventricular tachyarrhythmia in HCM patients and may provide a new phenotypic marker for adverse prognosis, especially in the intermediate risk group. Further studies in larger populations are required to assess its possible prognostic value.