Effects of cardiac rehabilitation on cardiopulmonary test parameters in heart failure: A real world experience.

Background: Cardio-Pulmonary Exercise Test (CPET) is the gold standard for evaluation of patients with heart failure (HF); however, its use is limited in everyday practice. We analyzed the use of CPET for HF management in the real world. Methods: From 2009 to 2022, 341 patients with HF underwent 12-16 weeks of rehabilitation in our Centre. We present data from 203 patients (60%), excluding those unable to perform CPET, those with anaemia and severe pulmonary disease. Before and after rehabilitation, we performed CPET, blood tests and echocardiography, tailoring individual physical training to the results of baseline test. The following variables were considered: peak Respiratory Equivalent Ratio (RER), peakVO2 (ml/Kg/min), VO2 at aerobic threshold (VO2AT,% maximal), VE/VCO2 slope, P(ET)CO2, VO2 /Work ratio (ΔVO2/ΔWork). Results: Rehabilitation improved peak VO2, pulse O2, VO2 AT and ΔVO2/ΔWork in all patients by about 13% (p < 0.01). Most patients (126, 62%) showed a reduced left ventricular ejection fraction (HFrEF), but rehabilitation was effective also in patients with mildly reduced (HFmrEF: n = 55, 27%) or preserved ejection fraction (HFpEF: n = 22, 11%). Conclusions: Rehabilitation in patients with heart failure induces a significant recovery of cardiorespiratory performance easily assessed by CPET, that is applicable to the majority of them and should be used routinely in the programming and evaluating of cardiac rehabilitation programs.

Do the remodeling effects of sacubitril/valsartan treatment depend upon heart failure duration?

AIMS: The angiotensin receptor and neprilysin inhibitor (ARNI) sacubitril/valsartan (LCZ696) is recommended for the treatment of patients with heart failure in New York Heart Association (NYHA) class II-III and left ventricular ejection fraction (LVEF) 35% or less. We examined the effects of sacubitril/valsartan on cardiac remodeling and their correlation with heart failure duration in patients enrolled in our heart failure clinic from March 2017 to December 2019. METHODS: Echocardiographic and clinical/laboratory data were collected at baseline and at 6-month and 12-month follow-up visits in 69 patients (age 67 ±â€Š12 years, disease duration 8.4 ±â€Š5.8 years, 93% men). RESULTS: At both time points, mean NYHA class, NT-proBNP level, LVEF, LV end-systolic volume, and estimated systolic pulmonary pressure significantly (P < 0.05) improved versus baseline, as did the proportion of patients with diastolic dysfunction grade 3 or functional mitral regurgitation grade 3-4. In the subgroup with mean disease duration less than 8.5 years (n = 40), there was a significant improvement in all variables at both time points; in this group, a recovery of right ventricular function was also seen at the 12-month follow-up. On the contrary, patients with heart failure duration of at least 8.5 years (n = 29) showed only a slight improvement in LVEF and mitral regurgitation at 12 months. There were no significant changes in renal function and/or potassium levels in all patients. CONCLUSION: In patients with a relatively short disease duration, sacubitril/valsartan was associated with a strong favorable remodeling of the left ventricle and improvement in pulmonary circulation.

[Safety and efficacy of early discharge and outpatient rehabilitation after myocardial infarction for low-risk patients]. / Sicurezza ed efficacia della dimissione precoce associata a riabilitazione ambulatoriale dopo infarto miocardico nel paziente a basso rischio.

BACKGROUND: Guidelines recommend early discharge and rehabilitation after ST-elevation myocardial infarction (STEMI) in low-risk patients. However, low risk is not established according to well-defined criteria and often it depends on subjective judgment. The aim of this real-life study is to confirm that early discharge is safe in patients at low risk according to selected criteria and subsequent outpatient rehabilitation is associated with clinical benefits. METHODS: Patients with STEMI treated with primary percutaneous coronary intervention from October 2010 to October 2017, identified as being at low risk (according to predefined criteria), discharged by day 5, were studied retrospectively. Basal characteristics and 30-day outcome were evaluated and a comparison was made between patients who completed or did not complete outpatient rehabilitation. RESULTS: We enrolled 193 STEMI patients treated with percutaneous coronary intervention for STEMI, early discharged and at low risk: 132 completed outpatient rehabilitation and 61 did not. The increase in cardiac enzymes and the occurrence of arrhythmias were the only independent predictors of completion of outpatient rehabilitation. After 30 days from discharge, adverse events were rare and not significantly different between groups. Optimal pharmacological therapy was achieved more often in the rehabilitation group (58.3% vs 44.3%; p<0.05). CONCLUSIONS: Early discharge within 5 days of STEMI has been proved feasible and safe in our population of well-defined low-risk patients. Early participation in a rehabilitation program was associated with a more adequate titration of therapy.

Long-term outcomes in difficult-to-treat patients with recurrent pericarditis.

Patients with many recurrences of acute pericarditis are commonly alarmed by the fear of constriction. We studied their long-term outcome and the possible presence of systemic diseases. Sixty-one Italian patients (36 men) were followed for an average of 8.3 years according to a predefined protocol, including testing for autoimmune diseases and familial Mediterranean fever. Symptomatic pericarditis lasted from 1 to 43 years (mean 5.4 years). Fifty-two patients had been referred to us after failure of previous therapies, including steroids. We observed 378 attacks with a mean of 1.6 per patient per year and 156 hospital admissions. Thirteen patients had a post-cardiac injury syndrome. In 43 (70.5%), the pericarditis remained idiopathic, whereas we made a new diagnosis of rheumatoid arthritis in 1 and of Sjogren's syndrome in 4 patients, but in these patients pericarditis represented the dominant clinical manifestation. Cardiac tamponade occurred during the initial attacks in 4 patients (6.5%) but never recurred. Pleural effusions were present during the first attack in 22 patients (36.0%) and liver involvement in 5 (8%). No patients developed constrictive pericarditis. Echocardiographic examination produced no evidence of chronic myocardial disease. Response to therapy was good. Thirty-one patients (50.8%) are in sustained remission, without any therapy; their total observation period has averaged 10.3 years. In idiopathic patients, antinuclear antibodies were present in 56.2% and anti-Ro/SSA in 8.3%. Mutations linked to familial Mediterranean fever were absent. In conclusion, in this large series of difficult patients with recurrent acute pericarditis and a very long follow-up, the long-term prognosis is good.

Neuronal nitric oxide synthase and renin stimulation by sodium deprivation are dependent on the renal nerves.

OBJECTIVE: The aim of the present study was to evaluate the role of the renal nerves in the regulation of neuronal nitric oxide synthase (nNOS) gene expression in normotensive rats on different sodium balance. METHODS: Thirty-six male Sprague-Dawley rats were divided into six experimental groups combining three diets with different NaCl content (normal, 0.4%; low, 0.04%; or high, 4.0%), and bilateral renal denervation or sham denervation. After 7 days of dietary treatment, all rats were sacrificed and plasma renin activity (PRA) measured. The nNOS and renin messenger RNA (mRNA) levels in the renal cortex were determined by semiquantitative polymerase chain reaction. RESULTS: PRA was higher in animals with low sodium diet compared with those with standard diet, while it was lower in animals with high sodium diet. Renal denervation decreased PRA in normal and low sodium groups, while it did not alter the PRA values in the high sodium group. The nNOS gene expression significantly increased in rats fed with the low sodium diet compared with the standard diet group, and it significantly decreased in rats with the high sodium diet. Renal denervation significantly reduced nNOS mRNA levels in rats receiving the low sodium diet, but did not significantly influence nNOS mRNA in normal and high sodium groups. Renin mRNA was influenced by diets and denervation in a parallel way to nNOS mRNA. CONCLUSION: The renal nerves mediate the increase of renin and nNOS mRNA during sodium restriction, while the suppression of nNOS and renin gene expression during a sodium load is independent of the presence of the renal nerves. The parallel changes in renin and nNOS mRNA during different sodium intakes suggest that nNOS can be part of the complex, and still largely unclarified, macula densa mechanism of renin regulation.