Management of cardiogenic shock complicating acute myocardial infarction: The Henry Ford Hospital experience and review of the literature.

Cardiogenic shock complicating acute myocardial infarction (MI) carries a high mortality which in some series prior to 1980 exceeded 80%. Neither the use of inotropic and vasopressor agents nor intraaortic balloon counterpulsation was found to improve survival in this group of patients. Intravenous thrombolytic agents improve survival in patients with acute MI, but their role in cardiogenic shock is unknown. Reports of the use of surgical and mechanical interventions in patients with severe left ventricular dysfunction were examined to determine if there was any benefit to be derived from restoring blood flow to ischemic areas of the myocardium. It was found that urgent placement of intraaortic balloon counterpulsation followed by coronary bypass surgery may improve survival rates and successful coronary angioplasty also appeared to benefit patients with cardiogenic shock. Similar improvement in survival has been reported after successful coronary reperfusion. In surgical series with predominantly nonmechanical causes of shock, survival has varied from 40% to 88%. Data from our five-year experience in the management of MI patients with cardiogenic shock suggest that coronary revascularization with coronary angioplasty or bypass surgery improves survival in patients with cardiogenic shock especially when performed within 24 hours of the onset of shock.     

Role of vasopressin antagonists in the management of acute decompensated heart failure

Vasopressin antagonists are a class of neurohormonal antagonists with applications in both the short-term and long-term management of patients with acute decompensated heart failure (ADHF). The pharmacologic effects of vasopressin antagonists include changes in fluid balance and hemodynamics that may improve symptoms and outcomes in patients hospitalized with ADHF. With chronic therapy, vasopressin antagonists offer the potential to improve outcomes through a variety of mechanisms, including more effective treatment of congestion, preservation or improvement of renal function, or a reduction in the use of concomitant loop diuretic therapy. Several vasopressin antagonists are currently in advanced clinical trials for the treatment of ADHF, chronic stable heart failure, and hyponatremia.     

Acute heart failure syndromes: Potential strategies to improve post-discharge outcomes

Hospitalization for acute heart failure syndromes (AHFS) is a significant negative predictor of prognosis. Although patients' presenting symptoms generally improve throughout hospitalization in response to therapy, post-discharge event rates, defined as rehospitalization and/or mortality, remain unacceptably high. In the past decade, many lifesaving therapies for heart failure, such as beta-blockers, aldosterone antagonists, and cardiac resynchronization therapy (CRT), have been defined. Hospitalization presents a unique opportunity to implement these and other lifesaving therapies. However, these opportunities are often missed, perhaps because the traditional focus of hospitalization has been on symptom relief, not improvement of post-discharge outcomes. Although many therapies are now available, each needs to be tailored to each patient based on a proper assessment (eg, revascularization for those with severe coronary artery disease, CRT for those with wide QRS). Thorough cardiac assessment combined with tailored implementation may improve post-discharge outcomes. New strategies are needed to improve uptake of current best-evidence therapies to decrease the morbidity and mortality of AHFS.     

Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF): rationale and design

Heart failure (HF) affects >5 million patients in the United States, and its prevalence is increasing every year. Despite the compelling scientific evidence that angiotensin-converting enzyme inhibitors and β-blockers reduce hospitalizations and mortality rates in patients with HF, these lifesaving therapies continue to be underused. Several studies in a variety of clinical settings have documented that a significant proportion of eligible patients with HF are not receiving treatment with these guideline-recommended, evidence-based therapies. In patients hospitalized with HF, who are at particularly high risk for re-hospitalization and death, the initiation of β-blockers is often delayed because of concern that early initiation of these agents may exacerbate HF. Recent studies suggest that β-blockers can be safely and effectively initiated in patients with HF before hospital discharge and that clinical outcomes are improved. The Initiation Management Predischarge Process for Assessment of Carvedilol Therapy for Heart Failure (IMPACT-HF) trial demonstrated that pre-discharge initiation of carvedilol was associated with a higher rate of β-blocker use after hospital discharge, with no increase in hospital length of stay. In addition, there was no increase in the risk of worsening of HF. Studies of hospital-based management systems that rely on early (pre-discharge) initiation of evidence-based therapies for patients with cardiovascular disease have also found increases in post-discharge use of therapy and a reduction in the rates of mortality and hospitalization. On the basis of these pivotal studies, the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF) program is designed to improve medical care and education of hospitalized patients with HF and accelerate the initiation of evidence-based HF guideline recommended therapies by administering them before hospital discharge. A registry component, planned as the most comprehensive database of the hospitalized HF population focusing on admission to discharge and 60- to 90-day follow-up, is designed to evaluate the demographic, pathophysiologic, clinical, treatment, and outcome characteristics of patients hospitalized with HF. The ultimate aim of this program is to improve the standard of HF care in the hospital and outpatient settings and increase the use of evidence-based therapeutic strategies to save lives.     

Prevalence, clinical phenotype, and outcomes associated with normal B-type natriuretic Peptide levels in heart failure with preserved ejection fraction

B-type natriuretic peptide (BNP) is used widely to exclude heart failure (HF) in patients with dyspnea. However, most studies of BNP have focused on diagnosing HF with reduced ejection fraction (EF). The aim of this study was to test the hypothesis that a normal BNP level (≤100 pg/ml) is relatively common in HF with preserved EF (HFpEF), a heterogenous disorder commonly associated with obesity. A total of 159 consecutive patients enrolled in the Northwestern University HFpEF Program were prospectively studied. All subjects had symptomatic HF with EF >50% and elevated pulmonary capillary wedge pressure. BNP was tested at baseline in all subjects. Clinical characteristics, echocardiographic parameters, invasive hemodynamics, and outcomes were compared among patients with HFpEF with normal (≤100 pg/ml) versus elevated (>100 pg/ml) BNP. Of the 159 patients with HFpEF, 46 (29%) had BNP ≤100 pg/ml. Subjects with normal BNP were younger, were more often women, had higher rates of obesity and higher body mass index, and less commonly had chronic kidney disease and atrial fibrillation. EFs and pulmonary capillary wedge pressures were similar in the normal and elevated BNP groups (62 ± 7% vs 61 ± 7%, p = 0.67, and 25 ± 8 vs 27 ± 9 mm Hg, p = 0.42, respectively). Elevated BNP was associated with enlarged left atrial volume, worse diastolic function, abnormal right ventricular structure and function, and worse outcomes (e.g., adjusted hazard ratio for HF hospitalization 4.0, 95% confidence interval 1.6 to 9.7, p = 0.003). In conclusion, normal BNP levels were present in 29% of symptomatic outpatients with HFpEF who had elevated pulmonary capillary wedge pressures, and although BNP is useful as a prognostic marker in HFpEF, normal BNP does not exclude the outpatient diagnosis of HFpEF.