Right ventricular diameter predicts all-cause mortality in heart failure with preserved ejection fraction.

Left ventricular ejection fraction (EF) is helpful to differentiate heart failure (HF) phenotype in clinical practice. The aim of the study was to identify simple echocardiographic predictors of post-discharge all-cause mortality in hospitalized HF patients. Patients with acute HF (75 ± 9.8 years), classified in preserved (≥ 50%) and reduced (< 50%) EF (HFpEF and HFrEF, respectively), were enrolled. The mean follow-up period was of 25.4 months. Patients definitively analyzed were 135. At multivariate Cox model, right ventricular diameter (RVd), inferior vena cava diameter (IVCd) and blood urea nitrogen (BUN) resulted to be significantly associated with all-cause mortality in HFpEF (HR 2.4, p = 0.04; HR 1.06, p = 0.02; HR 1.02, p = 0.01), whereas, left atrial volume (LAV) was significantly associated with mortality in HFrEF (HR 1.06, p = 0.006). Excluding LAV from the model, only COPD remained an independent predictor of all-cause mortality (HR 2.15, p = 0.04) in HFrEF. At Kaplan-Meier analysis, no differences of survival between HFrEF and HFpEF were found, however, significantly increased all-cause mortality for higher values of basal-RVd, BUN, and IVCd (log-rank p = 0.0065, 0.0063, 0.0005) in HFpEF, and for COPD and higher LAV (log-rank p = 0.0046, p = 0.033) in HFrEF. These data are indicative that in patients hospitalized with HF, EF is not a suitable predictor of long-term all-cause mortality, whereas, right ventricular volumetric remodeling and IVCd have a prognostic role in HFpEF as well as LAV in HFrEF. Our study suggests that besides EF, other echocardiographic parameters are helpful to optimize the phenotyping and prognostic stratification of HF.

NT pro BNP plasma level and atrial volume are linked to the severity of liver cirrhosis.

BACKGROUND AND AIMS: Plasma levels of NT-pro-BNP, a natriuretic peptide precursor, are raised in the presence of fluid retention of cardiac origin and can be used as markers of cardiac dysfunction. Recent studies showed high levels of NT pro BNP in patients with cirrhosis. We assessed NT pro-BNP and other parameters of cardiac dysfunction in patients with cirrhosis, with or without ascites, in order to determine whether the behaviour of NT pro BNP is linked to the stage of liver disease or to secondary cardiac dysfunction. METHODS: Fifty eight consecutive hospitalized patients mostly with viral or NAFLD-related cirrhosis were studied. All underwent abdominal ultrasound and upper GI endoscopy. Cardiac morpho-functional changes were evaluated by echocardiography and NT-pro-BNP plasma levels determined upon admission. Twenty-eight hypertensive patients, without evidence of liver disease served as controls. RESULTS: Fifty eight cirrhotic patients (72% men) with a median age of 62 years (11% with mild arterial hypertension and 31% with type 2 diabetes) had a normal renal function (mean creatinine 0.9 mg/dl, range 0.7-1.06). As compared to controls, cirrhotic patients had higher NT pro-BNP plasma levels (365.2±365.2 vs 70.8±70.6 pg/ml; p<0.001). Left atrial volume (LAV) (61.8±26.3 vs 43.5±14.1 ml; p = 0.001), and left ventricular ejection fraction (62.7±6.9 vs. 65.5±4%,; p = 0.05) were also altered in cirrhotic patients that in controls. Patients with F2-F3 oesophageal varices as compared to F0/F1, showed higher e' velocity (0.91±0.23 vs 0.66±0.19 m/s, p<0.001), and accordingly a higher E/A ratio (1.21±0.46 vs 0.89±0.33 m/s., p = 0.006). CONCLUSION: NT-pro-BNP plasma levels are increased proportionally to the stage of chronic liver disease. Advanced cirrhosis and high NT-pro-BNP levels are significantly associated to increased LAV and to signs of cardiac diastolic dysfunction. NT pro-BNP levels could hence be an useful prognostic indicators of early decompensation of cirrhosis.

Early and personalized ambulatory follow-up to tailor furosemide and fluid intake according to congestion in post-discharge heart failure.

Congestive heart failure (CHF) worsening is a worldwide cause of rehospitalization and mortality, specially during the early period after hospitalization. Fluid accumulation plays a key role in the pathophysiology of both acute heart decompensation and disease progression. The effective use of drugs to maintain restored clinical stabilization in recently discharged patients is a difficult task, and it relies on matching the most appropriately tailored therapy to specific clinical profiles. However, no successful treatment has been shown to reduce post-discharge readmission. We evaluated in a case-control study the effectiveness of an early and personalized congestion-guided ambulatory program on medium-term (6 months) compensation in recently discharged CHF patients. Group A (22 patients) underwent a post-discharge close follow-up consisting of: an early clinic visit within 10 days; a second visit within 10 days after the first; and the other visits at month 1, 2, 3 after discharge. Controls (Group B, 21 patients) underwent a conventional ambulatory follow-up only at month 1, 2, 3 after discharge. The ambulatory approach in both groups was based on the monitoring of signs/symptoms of congestion and body weight, body hydration estimation by using bioelectrical impedance analysis (BIA) and laboratory data. This assessment was finalized to tailor furosemide and daily fluid intake at each visit to eliminate clinical or instrumental evidence of persistent congestion relieving the signs and symptoms. At 6 months, Group A was associated with a better clinical compensation (improved hydration state, lower BNP levels and congestion score), an improved quality of life, and reduced re-hospitalizations. We conclude that in CHF the early and personalized ambulatory follow-up based on congestion-guided treatment is effective to optimize management and maintain clinical stability in the post-discharge period.

Troponin I release after intravenous treatment with high furosemide doses plus hypertonic saline solution in decompensated heart failure trial (Tra-HSS-Fur).

BACKGROUND: High values of cardiac troponin in acute decompensated congestive heart failure (ADHF) identify patients at higher risk and worsened prognosis. A cardiac troponin increase during therapy indicates the need for more appropriate intervention, aimed at compensating cardiac disease and effectively minimizing myocardial wall stress and subsequent cytolysis. This study evaluated the effects of an intravenous high dose of furosemide with (group A) or without small volume hypertonic saline solution (HSS) (group B) on myocardial cytolysis in patients with ADHF. METHODS: A total of 248 consecutive patients with ADHF (148 men, mean age 74.9 ± 10.9 years) were randomly assigned to group A or B. Plasma levels of cardiac troponin-I, brain natriuretic peptide, glomerular filtration rate by Modification of Diet in Renal Disease formula, bioelectrical impedance analysis measurements, and delta pressure/delta time (dP/dt) rate were observed on admission and discharge for all patients. RESULTS: We observed a significant reduction of cardiac troponin in both groups and a significant improvement in renal function, hydration state, pulmonary capillary wedge pressure (P < .0001), end diastolic volume (P < .01), ejection fraction (P < .01), and dP/dt (P < .004) in group A. We also observed a significant reduction in body weight (64.4 vs 75.8 kg) (P < .001), cardiac troponin I (0.02 vs 0.31 ng/mL) (P < .0001) and brain natriuretic peptide (542 vs 1,284 pg/mL) (P < .0001), and hospitalization time (6.25 vs 10.2 days) (P < .0001) in the HSS group. CONCLUSIONS: These data demonstrate that intravenous high doses of furosemide do not increase myocardial injury and, in addition, when associated to HSS, significantly reduce cardiac troponin I release. This behavior is mirrored by the achievement of improved hemodynamic compensation at echocardiography and body hydration normalization.

Large hiatal hernia at chest radiography in a woman with cardiorespiratory symptoms.

Hiatal hernia (HH) is a frequent entity. Rarely, it may exert a wide spectrum of clinical presentations mimicking acute cardiovascular events such as angina-like chest pain until manifestations of cardiac compression that can include postprandial syncope, exercise intolerance, respiratory function, recurrent acute heart failure, and hemodynamic collapse. A 69-year-old woman presented to the emergency department complaining of fatigue on exertion, cough, and episodes of restrosternal pain with less than 1 hour of duration. Her medical history only included some episodes of bronchitis and no history of hypertension. The 12-lead electrocardiogram demonstrated sinus rhythm with right bundle-branch block. Laboratory tests, including cardiac troponin I, were within normal reference values. Chest radiography showed no significant pulmonary alterations and revealed in mediastinum a huge abnormal shadow overlapping the right heart compatible with a gastric bubble.The gastroscopy confirmed a large HH. A 2-dimensional transthoracic echocardiogram, using all standard and modified apical and parasternal views, revealed an echolucent mass, compatible with HH, compressing the right atrium. Also, it showed an altered left ventricular relaxation and a mild increase of pulmonary artery pressure (35 mm Hg). Spirometry showed a mild obstruction of the small airways, whereas coronary angiography showed normal coronary arteries. We concluded that the patient's symptomatology was related to the compressive effects of the large hiatal ernia, a neglected cause of cardiorespiratory symptoms. The surgical repair of HH was indicated.

Changes in estimating echocardiography pulmonary capillary wedge pressure after hypersaline plus furosemide versus furosemide alone in decompensated heart failure.

BACKGROUND: The aim of the study was to verify the effects of hypertonic saline solution (HSS) plus a high furosemide dose and light restriction of sodium intake compared with a high-dose infusion of furosemide alone on pulmonary capillary wedge pressure (PCWP), as determined by Doppler echocardiography and tissue Doppler imaging in patients suffering from decompensated heart failure. METHODS AND RESULTS: Consecutive patients in New York Heart Association functional class IV, unresponsive to oral high doses of furosemide up to 250-500 mg/d and/or combinations of diuretics, with ejection fraction <40%, serum creatinine <2 mg/dL, blood urea nitrogen ≤60 mg/dL, reduced urinary volume (<500 mL/24 h), and low natriuresis (<60 mEq/24 h) were randomized into 2 groups (double blind). The first group received a furosemide infusion (250 mg) plus HSS (150 mL 3.0% Na) bid and light Na restriction (120 mmol), and the second group received furosemide infusion (250 mg) twice daily, and low Na diet (80 mmol). The fluid intake of both groups was restricted (1 L/d). Body weight, whole-body bioelectrical impedance analysis (BIA), 24-hour urinary volume, and serum and urinary laboratory parameters were measured daily. Estimations of echocardiographic PCWP (Echo-PCWP) were detected on entry, 1 hour after concluding the initial treatment, and 6 days thereafter. A total of 133 patients (47 women and 86 men), aged 65-82 years, met the entry criteria.The HSS group revealed a significant increase in daily diuresis, natriuresis, and serum sodium compared with the furosemide group. Six days after treatment, renal function was significantly improved in the HSS group. Both groups showed a significant reduction in Echo-PCWP, but the HHS group revealed a faster reduction and significant lower values at 6 days compared with the group taking furosemide alone. We observed a positive correlation between values of Echo-PCWP and BNP and an inverse correlation between BIA parameters and Echo-PCWP. CONCLUSIONS: Our data show that the combination of high diuretic dose and HSS infusion plus light restriction in dietary sodium intake determine a more rapid and significant hemodynamic stabilization through the improvement of echo-PCWP, BNP levels, and BIA parameters than the group treated without HSS.

One-year renal and cardiac effects of bisoprolol versus losartan in recently diagnosed hypertensive patients: a randomized, double-blind study.

BACKGROUND AND OBJECTIVES: Hypertension is a significant cause of chronic renal injury and its effective treatment is capable of reducing the rate of renal failure. beta-Adrenoceptor antagonists (beta-blockers) have been reported to induce a deterioration in renal function, while several data have indicated a renoprotective effect of treatment with the angiotensin II type 1 receptor antagonist losartan. Previous studies of the interaction between the selective beta(1)-blocker bisoprolol and kidney function were performed only for short- and medium-term periods. The aim of this study was to compare the antihypertensive efficacy and renal and cardiac haemodynamic effects of bisoprolol with those of losartan over a 1-year time period in patients with essential hypertension. METHODS: Seventy-two patients (40 males) with recently diagnosed uncomplicated (European Society of Hypertension [ESH] criteria stage 1-2) hypertension (mean +/- SD age 52 +/- 12 years) were enrolled in the study. After a run-in period of 14 days on placebo, the patients were randomized in a double-blind, prospective study to receive either bisoprolol 5 mg or losartan 50 mg, administered once daily for 1 year. At recruitment and 12 months after treatment, cardiac output and renal haemodynamics and function were evaluated by echocardiography and radionuclide studies, respectively. RESULTS: There were no significant differences in baseline clinical data, including glomerular filtration rate and blood pressure, between the two treatment groups. At 1 year, blood pressure had decreased significantly (p < 0.001) with both treatments, and heart rate was reduced only in the group taking bisoprolol. The long-term effects on renal haemodynamics and cardiac function were similar with both drugs, the only change being a significant reduction in the filtration fraction for each group. CONCLUSIONS: These data suggest that both bisoprolol and losartan are effective agents for the treatment of patients with recently diagnosed ESH stage 1-2 hypertension. Over a 1-year period, both agents maintained good renal and cardiac performance and haemodynamics.