The epidemiology of pulmonary hypertension (PH), especially pulmonary arterial hypertension (PAH), has not been evaluated in our country, therefore there is no reference parameter to establishing the ...representativeness of this information in the national order. This registry represents the first collaborative effort to provide a knowledge base of this disease, including 5 scientific societies that represent different specialties (pediatrics, rheumatology, pulmonology and cardiology) with data from 23 Argentine provinces. These efforts involved five societies of various adult (cardiology, rheumatology, and pulmonology) and pediatric (cardiology) specialties. Subjects were grouped (1-5) in accord with the 2013 Nice classification. A total of 627 patients (mean age, 50.8 ± 18 years; women, 69.2%) were recruited. Incident cases accounted for 53%. Functional class III-IV accounted for 69% at time of diagnosis and 33.4% at time of inclusion. Distributions in groups 1-5 were 63.6%, 15.9%, 8.3%, 9.7%, and 2.4%, respectively. Treatment consisted of diuretics (51.2%), mineralocorticoid receptor antagonists (44.7%), digoxin (16.6%), anticoagulants (39.2%), renin-angiotensin antagonists (15.5%), beta blockers (15.6%), and calcium channel blockers (8%). Rates of specific therapies usage in PAH vs. non-PAH group were 80.5% vs. 40.8% (phosphodiesterase-5 inhibitors: 71% vs. 38.6%; endothelin receptor antagonists: 54.4% vs. 14.5%; prostanoids: 14.3 vs. 3.1%; all p < 0.001). Three-year survival in PAH and non-PAH differed significantly (82.8% vs. 73.3%; p = 0.001). In the Argentine RECOPILAR registry, the clinic-epidemiologic profile was that of advanced-stage disease. Diagnostic workups and therapeutics interventions, including use of specific therapy for PAH, were consistent with current recommendations. Despite delays in diagnosis, survival was aligned with other contemporary registries.
C-reactive protein (CRP) levels are associated with cardiovascular risk. We assessed the hypothesis that atorvastatin might have anti-inflammatory effects in acute coronary syndromes (ACS) as shown ...by CRP reduction.
This study was a prospective, randomized, double-blind, placebo-controlled study of 90 consecutive patients admitted within 48 hours of onset of ACS with CRP levels ≥1.4 mg/dL. Patients were assigned to atorvastatin 40 mg daily or placebo over 30 days. C-reactive protein levels, lipid profiles, serum fibrinogen, white cell count, and erythrocyte sedimentation rate were measured at entry, hospital discharge, and 1 month later.
Baseline clinical characteristics did not differ between atorvastatin and placebo groups (mean age 59.3 ± 13.4 vs 61.1 ± 11.5,
P = ns); myocardial infarction 52.3% versus 67.4% (
P = ns). In both groups, median baseline CRP levels were comparable (5.97 ± 6.2 vs 4.64 ± 4.2 mg/dL,
P = ns). C-reactive protein levels were lower in the atorvastatin group versus control group at discharge (1.68 ± 1.65 vs 4.12 ± 4.18 mg/dL) and at 30 days (0.50 ± 0.71 vs 2.91 ± 2.68 mg/dL, both
P < .0001). C-reactive protein levels significantly decreased from baseline to discharge and 1 month later in placebo and atorvastatin groups (both
P < .0001); however, the reduction was greater in the atorvastatin group (62% vs 11% at discharge
P < .0001; 84% vs 30% at 1 month
P < .0001). In addition, atorvastatin was associated with a reduction in total and low-density lipoprotein cholesterol and erythrocyte sedimentation rate at discharge and at 30 days (
P < .0001 for all comparisons). No correlation was found between changes in CRP and cholesterol levels.
C-reactive protein levels in ACS were rapidly reduced with atorvastatin. These data provide evidence that statins have fast and early anti-inflammatory effects in addition to lipid-lowering effects in ACS.
Abstract Background Half of patients with acute heart failure syndromes (AHFS) have preserved left ventricular ejection fraction (PLVEF). In this setting, the role of minor myocardial damage (MMD), ...as identified by cardiac troponin T (cTnT), remains to be established. Aim To evaluate the prevalence and long-term prognostic significance of cTnT elevations in patients with AHFS and PLVEF. Patients and Methods This retrospective, multicenter, collaborative study included 500 patients hospitalized for AHFS with PLVEF (ejection fraction ≥40%) between October 2000 and December 2006. Blood samples were collected within 12 hours after admission and were assayed for cTnT. MMD was defined as a cTnT value of ≥0.020 ng/mL. Results Mean age was 73 ± 12 years, 47% were female, 38% had an ischemic etiology, and New York Heart Association (NYHA) class was 2.2 ± 0.7. Mean cTnT value was 0.149 ± 0.484 ng/mL, and cTnT was directly correlated with serum creatinine (Spearman's Rho = 0.35, P < .001) and NYHA class (0.25, P < .001). MMD was diagnosed in 220 patients (44%). Patients with MMD showed lower left ventricular ejection fraction ( P < .05), higher serum creatinine ( P < .001), higher prevalence of ischemic etiology and diabetes mellitus, a worse NYHA class ( P < .001), and higher natriuretic peptide levels ( P < .001) as compared with patients without MMD. At 6-month follow-up, overall event-free survival was 55% and 75% in patients with and without MMD ( P < .001), respectively. On multivariate Cox regression analysis, only NYHA class (HR = 1.50; P = .002) and MMD (HR = 1.81; P = .001) were identified as predictors of events. Conclusions Increased cTnT levels were detected in approximately 50% of patients with AHFS with preserved systolic function, and were found to correlate with clinical measures of disease severity. The presence of MMD was associated with a worse long-term outcome, lending support to cTnT-based risk stratification in the setting of AHFS.
Background: The progression of chronic heart failure (CHF) is characterized by frequent exacerbation requiring hospitalization and high mortality. Clinical deterioration is triggered by many factors ...that could promote ongoing myocytes injury. We sought to determine whether a specific marker of cardiac injury, troponin T (cTnT), is associated with prognosis in acute decompensated heart failure (ADHF).
Methods: One hundred and eighty-four consecutive patients with ADHF were enrolled in the absence of an acute coronary syndrome. A cTnT value≥0.1 ng/ml in samples drawn at 6, 12 or 24 h after hospital admission was considered abnormal.
Results: Increased levels of cTnT were found in 58 patients (31.5%, group 1). There were no significant differences between group 1 and patients with cTnT<0.1 ng/ml (group 2) in terms of demographic and clinical characteristics, although ischemic etiology was more prevalent in group 1 (51.7% vs. 31.7%,
p=0.009). During follow-up, the mortality in groups 1 and 2 was 31% and 17.5% (
p=0.038, OR=2.13, 95% CI: 1.03–4.69), respectively. The 3-year free-CHF readmission survival in group 1 and 2 was 25% and 53% (log rank test
p=0.015). In a Cox proportional hazard model, poor tissue perfusion (HR=2.46, 95% CI=1.31–4.6), previous infarction (HR=1.99, 95% CI=1.02–3.9) and cTnT≥0.1 ng/ml (HR=1.74, 95% CI=1.05–2.9) emerged as the independent predictors of long-term outcome.
Conclusions: One third of patients with decompensated CHF had elevated levels of cTnT. Troponin T was an independent long-term prognostic marker of morbidity and mortality and it suggests a role of biochemical risk stratification in this setting.
Tissue Doppler imaging (TDI) is useful in the evaluation of systolic and diastolic function. It allows assessment of ventricular dynamics in its longitudinal axis. We sought to investigate the ...difference in systolic and diastolic longitudinal function in patients with chronic heart failure (CHF) with normal and reduced ejection fraction.
One hundred ten outpatients with CHF and 68 controls were included. Ejection fraction (EF) was obtained and longitudinal systolic (
S) and diastolic (
E′ and
A′) wall velocities were recorded from basal septum. Group A (controls) were normal and CHF patients were classified by EF in Group B1: >
45% and B2: ≤
45%. In A, B1 and B2 the mean
S peak was 7.74; 5.45 and 4.89 cm/s (
p
<
0.001); the mean
E′ peak was 8.56; 5.72 and 6.1 cm/s (
p
<
0.001); and the mean
A′ peak was 10.2; 7.3 and 5.3 cm/s (
p
<
0.001). Also, isovolumic contraction and relaxation time were different among control and CHF groups, (both
p
<
0.001). The most useful parameters for identifying diastolic CHF were IVRT and
S peak, with area under ROC curves of 0.93 and 0.89. The cut-off of 115 ms for IVRT and 5.8 cm/s for
S peak showed a sensitivity of 94 and 97%, with a specificity of 82 and 73%, respectively.
These findings suggest that impairment of left ventricular systolic function is present even in those with diastolic heart failure, and that abnormalities may have an important role to identifying the condition.
Since early 2020, different studies have shown an increased prevalence of COVID-19 and poorer prognosis in older adults with cardiovascular comorbidities. This study aimed to assess the impact of ...heart failure (HF) on cardiovascular complications, intensive care unit (ICU) admissions, and in-hospital mortality in patients hospitalized with COVID-19. The CARDIO COVID 19-20 registry includes 3260 hospitalized patients with a COVID-19 serological diagnosis between May 2020 and June 2021 from Latin American countries. A history of HF was identified in 182 patients (5.6%). In patients with and without previous HF, the incidence of supraventricular arrhythmia was 16.5% vs. 6.3%, respectively (
= 0.001), and that of acute coronary syndrome was 7.1% vs. 2.7%, respectively (
= 0.001). Patients with a history of HF had higher rates of ICU admission (61.5% vs. 53.1%, respectively;
= 0.031) and in-hospital mortality (41.8% vs. 24.5%, respectively;
= 0.001) than patients without HF. Cardiovascular mortality at discharge (42.1% vs. 18.5%, respectively;
< 0.001) and at 30 days post-discharge (66.7% vs. 18.0%, respectively) was higher for patients with a history of HF than for patients without HF. In patients hospitalized with COVID-19, previous history of HF was associated with a more severe cardiovascular profile, with increased risk of cardiovascular complications, and poor in-hospital and 30-day outcomes.
Background: The COVID-19 pandemic has highlighted a correlation between cardiac complications and elevated cardiac biomarkers, which are linked to poorer clinical outcomes. Objective: This study aims ...to determine the clinical impact of cardiac biomarkers in COVID-19 patients in Latin America. Subjects and methods: The CARDIO COVID 19-20 Registry is a multicenter observational study across 44 hospitals in Latin America and the Caribbean. It included hospitalized COVID-19 patients (n = 476) who underwent troponin, natriuretic peptide, and D-dimer tests. Patients were grouped based on the number of positive biomarkers. Results: Among the 476 patients tested, 139 had one positive biomarker (Group C), 190 had two (Group B), 118 had three (Group A), and 29 had none (Group D). A directly proportional relationship was observed between the number of positive biomarkers and the incidence of decompensated heart failure. Similarly, there was a proportional relationship between the number of positive biomarkers and increased mortality. In Group B, patients with elevated troponin and natriuretic peptide and those with elevated troponin and D-dimer had 1.4 and 1.5 times higher mortality, respectively, than those with elevated natriuretic peptide and D-dimer. Conclusions: In Latin American COVID-19 patients, a higher number of positive cardiac biomarkers is associated with increased cardiovascular complications and mortality. These findings suggest that cardiac biomarkers should be utilized to guide acute-phase treatment strategies.
Background The clinical determinants of increased cardiac troponin T (cTnT) in patients with acute cardiogenic pulmonary edema are not well defined, and the ability of this marker to predict ...long-term mortality has not yet been documented. Methods Eighty-four patients with acute cardiogenic pulmonary edema without acute myocardial infarction were prospectively enrolled. cTnT was measured in samples obtained 6 and 12 hours after admission. Results cTnT levels of 0.1 ng/mL or greater were found in 46 patients (55%). Thirty-two patients (38%) died during follow-up. The area under the receiver operating characteristic curve for cTnT was 0.70 and 0.69 at 6 and 12 hours (P =.47), and the cTnT cutoff value of 0.1 ng/mL was 66% and 69% sensitive and 63% and 71% specific, respectively, in predicting subsequent mortality. Patients were assigned to group 1 if they had cTnT lower than 0.1 ng/mL and to group 2 if they had cTnT levels of 0.1 ng/mL or greater. A history of coronary artery disease was present in 72% of group 2 versus 50% of group 1 patients (P =.04). Patients in group 2 were also older than those in group 1 (mean age, 68 years vs 61 years; P =.021). The 3-year survival in group 1 was 76% compared with 29% in group 2 (log-rank test, P <.001). In a Cox proportional hazards model, elevated cTnT emerged as the only prognostic marker of long-term mortality (risk ratio RR = 2.31; 95% CI, 1.011-5.280; P =.047). Conclusions A cTnT level of 0.1 ng/mL or greater was associated with poor long-term survival and emerged as a powerful independent predictor of mortality in patients with acute cardiogenic pulmonary edema. (Am Heart J 2002;143:814-20.)
Heart failure with preserved ejection fraction is increasing in prevalence and is associated with a high symptom burden and functional impairment, especially in persons with obesity. No therapies ...have been approved to target obesity-related heart failure with preserved ejection fraction.
We randomly assigned 529 patients who had heart failure with preserved ejection fraction and a body-mass index (the weight in kilograms divided by the square of the height in meters) of 30 or higher to receive once-weekly semaglutide (2.4 mg) or placebo for 52 weeks. The dual primary end points were the change from baseline in the Kansas City Cardiomyopathy Questionnaire clinical summary score (KCCQ-CSS; scores range from 0 to 100, with higher scores indicating fewer symptoms and physical limitations) and the change in body weight. Confirmatory secondary end points included the change in the 6-minute walk distance; a hierarchical composite end point that included death, heart failure events, and differences in the change in the KCCQ-CSS and 6-minute walk distance; and the change in the C-reactive protein (CRP) level.
The mean change in the KCCQ-CSS was 16.6 points with semaglutide and 8.7 points with placebo (estimated difference, 7.8 points; 95% confidence interval CI, 4.8 to 10.9; P<0.001), and the mean percentage change in body weight was -13.3% with semaglutide and -2.6% with placebo (estimated difference, -10.7 percentage points; 95% CI, -11.9 to -9.4; P<0.001). The mean change in the 6-minute walk distance was 21.5 m with semaglutide and 1.2 m with placebo (estimated difference, 20.3 m; 95% CI, 8.6 to 32.1; P<0.001). In the analysis of the hierarchical composite end point, semaglutide produced more wins than placebo (win ratio, 1.72; 95% CI, 1.37 to 2.15; P<0.001). The mean percentage change in the CRP level was -43.5% with semaglutide and -7.3% with placebo (estimated treatment ratio, 0.61; 95% CI, 0.51 to 0.72; P<0.001). Serious adverse events were reported in 35 participants (13.3%) in the semaglutide group and 71 (26.7%) in the placebo group.
In patients with heart failure with preserved ejection fraction and obesity, treatment with semaglutide (2.4 mg) led to larger reductions in symptoms and physical limitations, greater improvements in exercise function, and greater weight loss than placebo. (Funded by Novo Nordisk; STEP-HFpEF ClinicalTrials.gov number, NCT04788511.).
