Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: A report from the shock trial registry

Potential Role of Humoral Immunity in Cardiac Dysfunction of Patients Suffering From Dilated Cardiomyopathy

(p⫽0.002), ejection fraction (p⫽0.013), and pulmonary artery systolic pressure (p⫽0.047) were all associated with in-hospital mortality. Using multivariate analysis the investigators found that both lower CPO (odds ratio [OR] per 0.20 W: 0.60 [95% CI, 0.44 – 0.83], p⫽0.002; n⫽181) and CPI (OR per 0.10 W/m2: 0.65 [95% CI, 0.48 – 0.87], p⫽0.004; n⫽178) were the strongest independent hemodynamic correlates of in-hospital mortality (after adjusting for age and history of hypertension). Age correlated inversely with CPI. Also, men had a higher CPI than did women. After adjusting for age, female gender continued to correlate with CPI (p⫽0.032). Conclusions: The researchers concluded that poor CPO is an important predictor of in-house mortality in patients with cardiogenic shock. They also found that CPO is lower in women and in older individuals. Perspective: The CPO is a novel hemodynamic yardstick incorporating both pressure and flow components of the heart’s pumping ability, and this study shows its utility in patients with shock. It would be interesting to study whether this hemodynamic measure remains a strong predictor at higher blood pressures. RB

Staudt A, Staudt Y, Do¨rr M, et al. J Am Coll Cardiol 2004;44: 829 –36. Study Question: What is the role of humoral immunity in dilated cardiomyopathy (DCM)? Methods: Circulating autoantibodies were purified from 45 DCM (LVEF⬍30%) before immunoadsorption therapy (IA). The functional effects of these antibodies on calcium transients and systolic cell shortening of adult rat cardiomyocytes were analyzed. Following this analysis, the patients underwent four courses of IA therapy at 1-month intervals. Results: The investigators identified two groups: a) the cardiodepressant group (n⫽29) whose antibodies induced a reduction (⬎10%) in calcium transients (mean reduction: ⫺16.5⫾1.9%) and ⬎10% reduction of cell shortening (mean reduction: ⫺21.2⫾1.8%) on cardiomyocytes (p⬍0.001), and b) noncardiodepressant group (n⫽16). In the cardiodepressant group with first course, IA demonstrated an acute increase in cardiac index (CI) from 2.2⫾0.1 L/min/m2 to 2.9⫾0.1 L/min/m2 (p⬍0.001), whereas in the noncardiodepressant group no significant change occurred in cardiovascular hemodynamics. At the end of the 3 months of IA, LVEF increased only in the cardiodepressant group, from 20.8⫾1% to 30.5⫾1% (p⬍0.01). Conclusions: The study investigators concluded that humoral immunity plays a significant role in cardiac dysfunction of DCM. Perspective: This study suggests immunomodulation may benefit selected patients with DCM. However, further studies are required before it is clear whether such therapy will have incremental value to standard therapy as more patients in the cardiodepressant group were on beta-blocker and angiotensin-converting enzyme inhibitor therapy. RB

Hemodynamic Effects of Inhaled Nitric Oxide in Right Ventricular Myocardial Infarction and Cardiogenic Shock Inglessis I, Shin JT, Leporeet JJ, et al. J Am Coll Cardiol 2004; 44:793–98. Study Question: The investigators sought to determine whether or not inhaled nitric oxide (NO) could improve hemodynamic function in patients with right-ventricular myocardial infarction (RVMI) and cardiogenic shock (CS). Methods: Thirteen patients (7 males and 6 females, age 65⫾3 years) presenting with electrocardiographic, echocardiographic, and hemodynamic evidence of acute inferior myocardial infarction associated with RVMI and CS were studied. After administration of supplemental oxygen (inspired oxygen fraction [FiO2]⫽1.0), hemodynamic measurements were recorded before, during inhalation of NO (80 ppm at FiO2⫽0.90) for 10 min, and 10 min after NO inhalation was discontinued (FiO2⫽1.0). Results: Breathing NO decreased the mean right atrial pressure by 12⫾3%, mean pulmonary arterial pressure by 13⫾2%, and pulmonary vascular resistance by 36⫾8% (all p⬍0.05). Nitric oxide inhalation increased the cardiac index by 24⫾11% and the stroke volume index by 23⫾12% (p⬍0.05). The NO administration did not change systemic arterial or pulmonary capillary wedge pressures. Contrast echocardiography identified three patients with a patent foramen ovale and right-to-left shunt flow while breathing at FiO2⫽1.0. Breathing NO decreased shunt flow by 56⫾5% (p⬍0.05) and was associated with markedly improved systemic oxygen saturation.

Cardiac Power Is the Strongest Hemodynamic Correlate of Mortality in Cardiogenic Shock: A Report From the SHOCK Trial Registry Fincke R, Hochman JS, Lowe AM, et al. for the SHOCK Investigators. J Am Coll Cardiol 2004;44:340 – 8. Study Question: How good a predictor of mortality is cardiac power in patients with cardiogenic shock (defined as the product of mean arterial pressure and cardiac output)? Methods: Cardiac power (CPO) and cardiac power index (CPI, product of mean arterial pressure and cardiac index) were calculated in 541 patients with cardiogenic shock. Results: Using univariate analysis the investigators found that CPO, CPI, cardiac output, cardiac index, stroke volume, left ventricular work, left ventricular work index, stroke work, mean arterial pressure, systolic and diastolic blood pressure (all p⬍0.001), coronary perfusion pressure

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