Olga Milo

Posttraumatic stress, nonadherence, and adverse outcome in survivors of a myocardial infarction.

Objective: Posttraumatic stress disorder (PTSD) symptoms have been reported in patients with coronary vascular disease, after the trauma of a myocardial infarction (MI). The effect of these symptoms on post-MI disease control has not been elucidated. We conducted a study that sought to determine whether PTSD symptoms post-MI are associated with increased likelihood of cardiovascular readmission and with nonadherence to treatment recommendations. Methods: Patients were recruited during a visit in a cardiology clinic 6 months post-MI and were followed for 1 year. Adherence to aspirin was measured by platelet thromboxane production (an indication of aspirins effect). Medical outcome was measured as rate of admission due to cardiovascular causes during the follow-up period. Self-report measures of PTSD (Impact of Event Scale), Depression, and Global Distress (SCL-90-R) were administered at enrollment. Results: Seventy-three patients were studied. Above-threshold PTSD symptom scores at enrollment, but not depression or global distress scores, were significant predictors of nonadherence to aspirin and of an increased likelihood of cardiovascular readmission over the course of the following year. Conclusions: PTSD symptoms predicted poor disease control in this cohort of MI survivors. The data suggest that screening MI survivors for symptoms of PTSD may be beneficial if this high-risk population is to be targeted for interventions.

The role of cardiac power and systemic vascular resistance in the pathophysiology and diagnosis of patients with acute congestive heart failure.

Conventional hemodynamic indexes (cardiac index (CI), and pulmonary capillary wedge pressure) are of limited value in the diagnosis and treatment of patients with acute congestive heart failure (CHF).

LINCS: L-NAME (a NO synthase inhibitor) in the treatment of refractory cardiogenic shock a prospective randomized study

AIMS To evaluate the effect of L-NAME (a nitric oxide synthase inhibitor) in the treatment of refractory cardiogenic shock. METHODS AND RESULTS We enrolled 30 consecutive patients with refractory cardiogenic shock (systolic blood pressure that deteriorated progressively to <100 mmHg during an acute coronary syndrome despite maximal percutaneous coronary revascularization, intra aortic balloon pump, and IV dopamine, furosemide and fluids treatment for at least 1h, accompanied by signs of peripheral hypoperfusion). Patients were randomized to supportive care alone (n=15, control group) or to supportive care in addition to L-NAME (1mg/Kg bolus and 1mg/Kg/h continuous IV drip for 5h n=15). Death at one month was 27% in the L-NAME group vs. 67% in the control group (p=0.008). Unaugmented mean arterial blood pressure at 24 h from randomization was 86+/-20 mmHg in the L-NAME group vs. 66+/-13 mmHg in the control group (p=0.004). Urine output increased at 24h by 135+/-78 cc/h in the L-NAME group vs a decrease of 12+/-87 cc/h in the control group (p<0.001). Time on IABP and time on mechanical ventilation were significantly shorter in the L-NAME group. CONCLUSIONS The results of the present study further support our previous observation that NO synthase inhibitors are beneficial in the treatment of patients with refractory cardiogenic shock.

RITZ-5: randomized intravenous TeZosentan (an endothelin-A/B antagonist) for the treatment of pulmonary edema. A prospective, multicenter, double-blind, placebo-controlled study ☆

OBJECTIVES The objective of this study was to evaluate the addition of intravenous (IV) tezosentan to standard therapy for patients with pulmonary edema. BACKGROUND Tezosentan is an IV nonselective endothelin (ET)-1 antagonist that yields favorable hemodynamic effects in patients with acute congestive heart failure (CHF). METHODS Pulmonary edema was defined as acute CHF leading to respiratory failure, as evidenced by an oxygen saturation (SO(2)) <90% by pulse oxymeter despite oxygen treatment. All patients received oxygen 8 l/min through a face mask, 3 mg of IV morphine, 80 mg of furosemide, and 1 to 3 mg/h continuous drip isosorbide-dinitrate according to their blood pressure level and were randomized to receive a placebo or tezosentan (50 or 100 mg/h) for up to 24 h. RESULTS Eighty-four patients were randomized. The primary end point, the change in SO(2) from baseline to 1 h, was 9.1 +/- 6.3% in the placebo arm versus 7.6 +/- 10% in the tezosentan group (p = NS). The incidence of death, recurrent pulmonary edema, mechanical ventilation, and myocardial infarction during the first 24 h of treatment was 19% in both groups. Reduced baseline SO(2), lower echocardiographic ejection fraction, high baseline mean arterial blood pressure (MAP), and inappropriate vasodilation (MAP reduction at 30 min of <5% or >30%) correlated with worse outcomes. A post-hoc analysis revealed that the outcome of patients who received only 50 mg/h tezosentan was better than patients in the placebo group whereas patients receiving 100 mg/h had the worst outcomes. CONCLUSIONS In the present study, tezosentan (an ET-1 antagonist) did not affect the outcome of pulmonary edema, possibly because of the high dose used.

A randomized, double-blind, placebo-controlled, multicentre study to assess haemodynamic effects of serelaxin in patients with acute heart failure

Aims The aim of this study was to evaluate the haemodynamic effects of serelaxin (30 µg/kg/day 20-h infusion and 4-h post-infusion period) in patients with acute heart failure (AHF). Methods and results This double-blind, multicentre study randomized 71 AHF patients with pulmonary capillary wedge pressure (PCWP) ≥18 mmHg, systolic blood pressure (BP) ≥115 mmHg, and estimated glomerular filtration rate ≥30 mL/min/1.73 m2 to serelaxin (n = 34) or placebo (n = 37) within 48 h of hospitalization. Co-primary endpoints were peak change from baseline in PCWP and cardiac index (CI) during the first 8 h of infusion. Among 63 patients eligible for haemodynamic analysis (serelaxin, n = 32; placebo, n = 31), those treated with serelaxin had a significantly higher decrease in peak PCWP during the first 8 h of infusion (difference vs. placebo: −2.44 mmHg, P = 0.004). Serelaxin showed no significant effect on the peak change in CI vs. placebo. Among secondary haemodynamic endpoints, a highly significant reduction in pulmonary artery pressure (PAP) was observed throughout the serelaxin infusion (largest difference in mean PAP vs. placebo: −5.17 mmHg at 4 h, P < 0.0001). Right atrial pressure, systemic/pulmonary vascular resistance, and systolic/diastolic BP decreased from baseline with serelaxin vs. placebo and treatment differences reached statistical significance at some time points. Serelaxin administration improved renal function and decreased N-terminal pro-brain natriuretic peptide levels vs. placebo. Treatment with serelaxin was well tolerated with no apparent safety concerns. Conclusion The haemodynamic effects of serelaxin observed in the present study provide plausible mechanistic support for improvement in signs and symptoms of congestion observed with this agent in AHF patients. ClinicalTrials.gov identifier NCT01543854.

Recent developments in cardiac output determination by bioimpedance: comparison with invasive cardiac output and potential cardiovascular applications.

Purpose of review To describe recent developments in bioimpedance technique and its application in cardiovascular diseases. Cardiac output determination has been used selectively during recent years because of the need for invasive right heart catheterization. Hence, experience with its application in patients with cardiovascular diseases and especially heart failure is limited. Bioimpedance is a novel noninvasive technique determining changes in instantaneous (during one heartbeat) conductance of a small electrical current transferred through the body. By using different algorithms correcting for various body composition constants, it calculates the change in instantaneous arterial blood volume (that is, stroke volume) and cardiac output. Traditionally, bioimpedance cardiac output is determined using either thoracic or whole body techniques according to the location of the electrodes transmitting and receiving the small electrical current. Recent findings Significant progress was achieved in recent years in cardiac output determination by bioimpedance. Newer algorithms using thoracic and whole body bioimpedance have demonstrated better correlation with invasive cardiac output determination. In a few preliminary studies bioimpedance-determined cardiac output was found useful in the diagnosis, risk stratification, and treatment titration of some cardiovascular conditions. Further, larger prospective studies are required to determine the true independent value of cardiac output measurement by bioimpedance for the evaluation of cardiovascular diseases and especially heart failure. Summary Recently, significant improvement was achieved in cardiac output measurement by bioimpedance with both newer thoracic and whole body techniques. Preliminary studies imply that this measure may be of value in managing some cardiovascular disorders.

Acute heart failure in the elderly: Differences in clinical characteristics, outcomes, and prognostic factors in the Veritas study

BACKGROUND Acute heart failure (HF) is common in the elderly, but the association of age with clinical outcomes and prognostic factors has not been examined thoroughly. METHODS AND RESULTS We analyzed the clinical and laboratory characteristics and the outcomes of 1,347 patients with acute HF enrolled in the VERITAS trial. Subjects were subdivided based on their median age of 72 years. Older patients had a higher prevalence of comorbidities and a higher prevalence of hypertension and atrial fibrillation. During a mean follow-up of 149 ± 61 days, 432 patients (32.1%) reached the composite end point of death, in-hospital worsening HF, or HF rehospitalization by 30 days, and 135 patients (10.4%) died by 90 days, with a worse outcome in elderly patients in both cases. At multivariable analysis, different variables were related with each of these outcomes in elderly compared with younger patients. Regarding deaths at 90 days, plasma urea nitrogen and hemoglobin levels were predictive only in the younger patients, whereas respiratory rate and albumin levels were associated with mortality only in the older patients. CONCLUSIONS Elderly patients with acute HF have different clinical characteristics and poorer outcomes. Prognostic variables differ in elderly compared with younger patients.

Growth differentiation factor 15 (GDF-15) in patients admitted for acute heart failure: results from the RELAX-AHF study.

Growth differentiation factor 15 (GDF‐15) was found to be upregulated in patients with chronic heart failure (HF) and associated with disease severity, however, data on patients with acute heart failure (AHF) is lacking.

Echocardiographic ejection fraction in patients with acute heart failure : correlations with hemodynamic, clinical, and neurohormonal measures and short-term outcome

Although echocardiographic ejection fraction (EF) is frequently used for the estimation of left ventricular contractility in patients with acute heart failure, its exact role and correlations with clinical, hemodynamic, and neurohormonal variables of cardiac contractility is not known.

Patient journey after admission for acute heart failure: length of stay, 30-day readmission and 90-day mortality.

The course of patients following admission for acute heart failure (AHF) is of major importance to patients and healthcare providers. We examined predictors and associations of length of stay (LOS), 30‐day post‐discharge readmission and 90‐day post‐discharge mortality in 1990 patients enrolled in the PROTECT study.