Characteristics, outcomes, and predictors of 1-year mortality in patients hospitalized for acute heart failure.

AIMS: Acute heart failure (AHF) is associated with poor prognosis and requires recurrent hospitalizations. However, studies on AHF characteristics, treatment, and prognostic factors are few. Our aim was to investigate the characteristics, treatment, and 1-year prognosis of AHF and identify prognostic factors in different clinical groups. METHODS AND RESULTS: We conducted a prospective multicentre study with 620 patients hospitalized due to AHF; mean age 75.1 (10.4) years, 50% male. Half of the patients had new-onset heart failure. Acute congestion (63.5%) and pulmonary oedema (26.3%) were the most common clinical presentations. Left ventricular ejection fraction (LVEF) was reported in two-thirds of patients. Half of these had preserved systolic function (LVEF> or =45%). At discharge, 86% of patients had beta-blockers and 76% either ACE-inhibitors or angiotensin receptor blockers in use. The 12-month all-cause mortality was 27.4%. We identified several clinical and biochemical prognostic risk factors in univariate analysis. Independent predictors of 1-year mortality were older age, male gender, lower systolic blood pressure (SBP) on admission, C-reactive protein, and serum creatinine >120 micromol/L. CONCLUSION: We present the characteristics and prognosis of an unselected population of AHF patients. One-year mortality is high, and independent clinical risk factors include age, male gender, lower SBP on admission, C-reactive protein, and renal dysfunction.     

Epidemiology,pathophysiology and contemporary management of cardiogenic shock – a position statement from the Heart Failure Association of the European Society of Cardiology

Cardiogenic shock (CS) is a complex multifactorial clinical syndrome with extremely high mortality, developing as a continuum, and progressing from the initial insult (underlying cause) to the subsequent occurrence of organ failure and death. There is a large spectrum of CS presentations resulting from the interaction between an acute cardiac insult and a patient's underlying cardiac and overall medical condition. Phenotyping patients with CS may have clinical impact on management because classification would support initiation of appropriate therapies. CS management should consider appropriate organization of the health care services, and therapies must be given to the appropriately selected patients, in a timely manner, whilst avoiding iatrogenic harm. Although several consensus‐driven algorithms have been proposed, CS management remains challenging and substantial investments in research and development have not yielded proof of efficacy and safety for most of the therapies tested, and outcome in this condition remains poor. Future studies should consider the identification of the new pathophysiological targets, and high‐quality translational research should facilitate incorporation of more targeted interventions in clinical research protocols, aimed to improve individual patient outcomes. Designing outcome clinical trials in CS remains particularly challenging in this critical and very costly scenario in cardiology, but information from these trials is imperiously needed to better inform the guidelines and clinical practice. The goal of this review is to summarize the current knowledge concerning the definition, epidemiology, underlying causes, pathophysiology and management of CS based on important lessons from clinical trials and registries, with a focus on improving in‐hospital management.     

Cystatin C: a step forward in assessing kidney function and cardiovascular risk

The cardiorenal syndrome is a clinical manifestation of the bidirectional interaction between the heart and kidneys. Evaluating renal function is an essential part of the assessment of every cardiac patient. It has become clear that serum creatinine is not an accurate enough marker of glomerular filtration rate (GFR) and should not be used to evaluate kidney dysfunction. Creatinine-based estimates of GFR are preferred, but require renal function to be stable and are not suitable when changes in kidney function occur. Cystatin C (CysC) has been the target of much interest in the search for an alternative measure of GFR. As an endogenous biomarker, CysC possesses many of the properties required of a good marker of renal function. Compared with that of creatinine, plasma concentrations of CysC are less influenced by factors other than GFR. Consequently, CysC correlates with true GFR more accurately than creatinine. Equations for estimating GFR from CysC values have also been developed, which makes values easier to interpret and facilitates the clinical use of this new marker. The use of CysC in acute kidney injury has also shown promising results. CysC has been studied as a risk marker for prognosis in cardiovascular disease. This effect is attributed to the strong impact of renal dysfunction on progressive cardiovascular disease and impaired survival. Higher levels of CysC have consistently been predictive of incident or recurrent cardiovascular events and adverse outcomes. CysC is a predictor of the development of heart failure and increased levels of CysC have an independent association with higher mortality in both chronic and acute heart failure. In conclusion, CysC appears to be an interesting marker of renal function and is useful for risk stratification in heart failure.     

Traumatic rupture of the right hemidiaphragm

Sixteen cases of traumatic disruption of the right hemidiaphragm are presented. Six tears were treated in the acute post-trauma phase and ten were detected from late manifestations. The causal trauma was penetrating in 11 cases and blunt in five. Rupture of the right hemidiaphragm not uncommonly occurs without serious associated injuries. Bowel often herniates through such tears, unhindered by the liver, though the liver is the most commonly herniating organ. No recurrence of hernia was found after standard repair techniques (mean follow-up 5.2 years). Three of the 16 patients died, one from associated injury, one from strangulation of herniated bowel and one from postoperative myocardial infarction. To demonstrate diaphragmatic tearing and subsequent organ herniation, serial chest radiographs and computed tomography are useful, and exploratory laporotomy should be done without delay after penetrating injury to the trunk. The treatment of diaphragmatic tear is surgical, with better results from early than from late repair.     

Persistent improvement after coronary bypass surgery: ergometric and angiographic correlations at 5 years

One hundred patients with angina pectoris who fulfilled specific entry criteria were randomly assigned to either medical therapy or bypass surgery. These groups were subjected to annual exercise testing during a 5-year follow-up period. The degree of revascularization was assessed by graft and native vessel angiography at 3 weeks, 1 year and 5 years after the operation. The exercise tolerance of the medical group remained largely unchanged during the follow-up. Eighty-five to 95% of the patients were using beta-blocking compounds at the successive testing situations. The surgical group exhibited a sustained improvement in exercise tolerance: Total work increased by 39-66% (p less than 0.02-0.001) and maximal ergometric load by 23-35% (p less than 0.01-0.001), and maximal ST depression decreased by 39-61% (p less than 0.05-0.001). The use of beta-blocking compounds in the surgical group steadily increased, from 44% at 6 months after operation to 63% of patients at 5 years. Division of the surgical group into subsets of complete and incomplete revascularization revealed that the improvement was confined to complete revascularization. Thus, the improved exercise tolerance after bypass surgery was a result of successful reestablishment of effective coronary perfusion; despite graft attrition (15% in 5 years) and new lesions in the native arteries, this improvement persisted for 5 years with appropriate medical therapy.     

Preservation of venous valve function after catheter-directed and systemic thrombolysis for deep venous thrombosis.

OBJECTIVES: The aim of the study was to assess venous reflux and the obstruction pattern after catheter-directed and systemic thrombolysis of deep iliofemoral venous thrombosis. PATIENTS: Thirty-two patients treated either with systemic (16) or catheter-directed local thrombolysis (16) for massive iliofemoral thrombosis were identified from the hospital registry. METHODS: Clinical evaluation at follow up was based on the CEAP classification and disability score. Reflux was assessed by colour duplex ultrasonography and standardised reflux testing. A vascular surgeon blinded to treatment established the clinical status of the lower limb following the previous DVT. RESULTS: Valvular competence was preserved in 44% of patients treated with catheter-directed thrombolysis compared with 13% of those treated with systemic thrombolysis (p=0.049, Chi squared). Reflux in any deep vein was present in 44% of patients treated by catheter-directed lysis compared with 81% of patients receiving systemic thrombolysis (p=0.03, Chi squared). Reflux in any superficial vein was observed in 25% vs. 63% of the patients, respectively (p=0.03, Chi squared). There were significantly more patients with venous insufficiency of classes C0-1 in the group treated with catheter-directed thrombolysis. CONCLUSION: In this clinical series venous valvular function was better preserved after iliofemoral DVT when treated with catheter-directed thrombolysis.