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The Impella (Abiomed, Danvers, Massachusetts) device is increasingly used for mechanical circulatory support (MCS) to treat acute severe cardiogenic shock (CS). Initial and continued determination of the appropriate degree of MCS is challenging. This study evaluates predictors of mortality in patients treated with the Impella for acute severe CS and outcomes associated with prolonged Impella use. This retrospective single-center study included 204 patients treated with the Impella 2.5, Impella CP, or Impella 5.0 from 2011 to 2018 for acute severe CS. The primary end point was all-cause in-hospital mortality. All-cause in-hospital mortality was 45.1%. Nonsurvivors had a lower initial pH (7.24 vs 7.32, hazard ratio [HR] 1.03, p <0.0001), lower serum CO 2 (19.1 vs 21.3 mmol/L, HR 1.08, p = 0.002), higher lactate (6.8 vs 3.3 mmol/L, HR 1.17, p <0.0001), and used a greater number of vasopressors and inotropes (4.3 vs 2.6, HR 1.44, p <0.0001). Patients with the Impella >4 days (n = 45) had a longer intensive care unit stay (12.6 vs 6.9 days, p <0.001), longer total hospital stay (16.4 vs 11.6 days, p = 0.03), longer mechanical ventilation use (7.8 vs 4.4 days, p = 0.002), and trend toward increased mortality (57.8 vs 41.5%, p = 0.051). In conclusion, in patients treated with the Impella for acute severe CS, initial biochemical parameters and need for vasopressors and inotropes are significant predictors of mortality that can serve as valuable indicators of whether the Impella or higher level of MCS is more appropriate. Patients treated with the Impella beyond 4 days have poorer outcomes and may benefit from escalation of care., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

Cardiogenic shock (CS) is a cardiac emergency often leading to multiple organ failure and death. Assessing organ dysfunction and appropriate risk stratification are central for the optimal management of these patients. The purpose of this study was to assess the prevalence of abnormal liver function tests (LFTs), as well as early changes of LFTs and their impact on outcome in CS. We measured LFTs in 178 patients in CS from serial blood samples taken at 0 hours, 12 hours, and 24 hours. The associations of LFT abnormalities and their early changes with all-cause 90-day mortality were estimated using Fisher's exact test and Cox proportional hazards regression analysis. Baseline alanine aminotransferase (ALT) was abnormal in 58% of the patients, more frequently in nonsurvivors. Abnormalities in other LFTs analyzed (alkaline phosphatase, gamma-glutamyl transferase, and total bilirubin) were not associated with short-term mortality. An increase in ALT of >20% within 24 hours (ΔALT>+20%) was observed in 24% of patients. ΔALT>+20% was associated with a more than 2-fold increase in mortality compared with those with stable or decreasing ALT (70% and 28%, p <0.001). Multivariable regression analysis showed that ΔALT>+20% was associated with increased 90-day mortality independent of other known risk factors. In conclusion, an increase in ALT in the initial phase was seen in 1/4 of patients in CS and was independently associated with 90-day mortality. This finding suggests that serial ALT measurements should be incorporated in the clinical assessment of patients in CS., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Even in the era of primary percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI) complicated by cardiogenic shock (CS), mortality remains high. Whether admission hemoglobin (Hb) concentration is a predictor of mortality in patients with CS treated with primary PCI is unexplored. We assessed the relation between admission Hb concentration and 1-year mortality in patients with STEMI and CS who were treated with PCI at admission. We investigated a cohort of 265 patients with STEMI with CS on admission. Patients were categorized in 3 groups according to plasma Hb levels at admission: 9.6 g/dl (group I, n = 22), 9.6 to 12 g/dl (group II, n = 59), and >12 g/dl (group III, n = 184). All-cause mortality at 1 year was 64%, 46%, and 35% for groups I, II, and III, respectively (p = 0.007). Multivariate logistic regression analysis showed that the odds for mortality increased 17% for every 1.0 g/dl decrease in plasma Hb (odds ratio 1.17, 95% confidence interval 1.01 to 1.35, p = 0.042). In conclusion, admission Hb concentration is an independent predictor for 1-year mortality in patients with STEMI undergoing primary PCI.

Data were obtained and analyzed in 229 patients admitted to the coronary care unit from November 1988 through July 1989. The patients were classified into 2 groups: patients without or with only mild left ventricular failure (Killip class I or II) during their hospital stay (group I), and patients who were in Killip class I or II on admission but developed cardiogenic shock during hospitalization (group II). Discriminant function analysis was performed using the following variables: patients' age, history of previous myocardial infarction, diabetes mellitus, blood lactate, urea, creatinine, creatine kinase, aspartate aminotransferase, lactate dehydrogenase concentrations, and chest x-ray cardiothoracic ratio. Variables that were found to significantly discriminate the 2 groups of patients were age, previous infarction, x-ray cardiothoracic ratio, blood urea and lactate concentrations. The risk index was computed, and blood lactate was the variable with the greatest predictive power for shock development. The sensitivity, specificity and predictive value of the risk index, taking various cutoff points, were calculated. With a cutoff value of 1, sensitivity was 65%, specificity 91%, positive predictive value 36% and negative predictive value 97%. With a cutoff value of 2, sensitivity was 53%, specificity 99%, positive predictive value 82% and negative predictive value 96%.

The hepatic hemodynamic response to cardiogenic shock was investigated in a porcine model produced by pericardial tamponade to better understand the pathophysiology of postshock hepatic insufficiency. Reductions of cardiac output to 50 percent of baseline levels produced marked hepatic ischemia by causing disproportionate reductions in blood flow through the celiac and hepatic arteries and portal vein. These were due to selective vasoconstriction of the splanchnic resistance vessels that was mimicked without tamponade by the infusion of angiotensin II, ablated by angiotensin-converting enzyme blockade, unaffected by alpha-adrenergic ablation, and correlated closely with levels of plasma renin activity. The ischemic liver injury of cardiogenic shock appears to be largely due to an exquisite responsiveness of the splanchnic vascular smooth muscle to endogenously released angiotensin II.

Thirteen patients in severe cardiogenic shock, persisting despite the use of adrenergic agents, were treated with enoximone, a recently available phosphodiesterase inhibitor. Cardiogenic shock was characterized by low cardiac output (less than 2.5 liter.min-1.m-2), elevated pulmonary artery balloon-occluded pressure (greater than or equal to 15 mm Hg), decreased urine output (less than 20 ml.hour-1) and increased blood lactate (greater than or equal to 2.0 mEq.liter-1). Ten patients were mechanically ventilated. A short-term intravenous infusion of 0.5 mg.kg-1 in 20 minutes of enoximone resulted in significant increases in cardiac index (from 1.8 +/- 0.3 to 2.9 +/- 0.3 liter.min-1.m-2, p less than 0.001) and stroke index (from 17.8 +/- 3.3 to 21.9 +/- 5.1 ml.m-2, p less than 0.001) and significant decrease in pulmonary artery balloon-occluded pressure (from 21.7 +/- 5.8 to 19.8 +/- 6.0 mm Hg, p less than 0.01) without a consistent change in mean arterial pressure (from 79 +/- 8 to 76 +/- 9 mm Hg, difference not significant). Enoximone administration decreased arterial oxygen tension (from 108 +/- 42 to 94 +/- 36 mm Hg, p less than 0.01) and increased venous admixture (from 12.8 +/- 6.5 to 16.0 +/- 8.0%, p less than 0.01). In 8 patients, a second infusion of 0.5 mg.kg-1 immediately thereafter amplified these changes. All patients but one survived the episode of cardiogenic shock and 5 patients left the hospital alive. These results indicate that the addition of enoximone to adrenergic agents in the treatment of cardiogenic shock can markedly increase cardiac output and stroke volume without substantial effects on arterial pressure.

The aim of this study was to determine the oxigen affinity actually present in vivo in blood from patients with acute myocardial infarction. Patients with uncomplicated acute myocardial infarction had normal value of P50 in vivo (partial pressure of oxygen at which 50 percent of the hemoglobin is saturated with oxygen at fixed levels of pHand PC02 present in vivo). Also the values of P50 in vivo of blood from patients with low cardiac output with mild or severe heart failured did not differ from the normal mean. This was the consequence of an increase of 2, 3-diphosphoglycerate levels (which reduces the oxygen affinity of hemoglobin) and of the immediate effect of alkalosis (Bohr effect). By contrast, the values of P50 in vivo were significantly increased in patients with cardiogenic shock. This could be ascribed to the state of acute acidiosis present in these patients. In these conditions the changes in the values of P50 in vivo play an important role in the oxygen delivery to the tissues. However, high values of P50 do not enhance oxygen delivery when a severe arterial hypoxemia (P02 smaller than 40-45 mm Hg) is also present.

To determine whether the extensive myocardial injury associated with cardiogenic shock in some patients results from a progressive rather than a discrete massive insult, a study was made of 15 selected patients who had cardiogenic shock within 48 hours of admission, 5 patients with hypovolemic shock without myocardial infarction and 11 patients with myocardial infarction without shock. Peak plasma MB creatine kinase (CK) activity was significantly higher in the seven patients with cardiogenic shock associated with initial infarction (213 international units [IU]/liter) than in patients with shock and previous infarction (98 IU/liter) and in patients with uncomplicated myocardial infarction (125 IU/liter). A prolonged time to peak MB CK activity (averaging 26 hours) and a plateau of elevated MB CK activity were seen in patients with shock associated with initial infarction. Because shock itself did not slow the rate of apparent MB CK disappearance, results obtained suggest that cardiogenic shock associated with initial infarction in selected patients results from progressive myocardial damage underlying continuing release of MB CK into the circulation. The findings are compatible with the concept that, in these patients, cardiogenic shock reflects a vicious cycle of spreading myocardial injury, progressive compromise of cardiac function, exacerbation of ischemia and perpetuation of myocardial damage.

Changes in systemic oxygen delivery after acute myocardial infarction were investigated in 21 patients. In seven patients with shock, circulatory failure was characterized by a significant reduction in cardiac index, a decrease in oxygen transport and oxygen consumption and an increase in concentration of blood lactate; a decrease in the affinity of hemoglobin for oxygen (increased P50) was also noted. The P50 averaged 28.8 plus or minus 0.87 (standard error of the mean) torr in patients with shock and 26.0 plus or minus 0.45 torr (P less than 0.05) in patients without circulatory failure. However, there was no significant difference in oxygen extraction from arterial blood between the two groups. The time course of the changes in P50, cardiac index and oxygen consumption was separately examined in 12 patients. In six patients with shock, P50 increased by an average of 4.6 plus or minus 2.05 torr (P less than 0.05) and this augmentation accounted for an estimated 18 percent increase in oxygen release. Maximal P50 values were observed after 24 hours of circulatory failure. In the absence of shock, no consistent changes in P50, cardiac index or oxygen consumption were observed. These data indicate that a reduction in oxygen delivery after acute myocardial infarction is followed by a compensatory increase in P50. This change in P50 accounts for increases in oxygen availability independently of changes in cardiac output.

The effect of carotid sinus pressure (CSP) on sinus rate was studied in 24 patients with sinoatrial pauses below 3 sec (control) and 23 patients with sinoatrial pauses above 3 sec (hypersensitive carotid sinus reflex equal to (HCSR). For registration of P waves, intraatrial electrograms were used. CSP was applied several times before and after atropine. Patients with HCSR showed inconstant response to CSP. The maximal result was considered diagnostic. No difference in the lengths of sinoatrial pauses was found between patients without dizziness or syncopes in the presence of HCSR and patients with dizziness that proved clinically to be based on the existence of HCSR. It was concluded that CSP-induced asystole can serve neither as a differential diagnostic criterion nor as an indication for pacemaker application. Sick sinus syndrome, and thereby dysfunction of the sinus node, were excluded by rapid atrial stimulation. Patients with HCSR showed overall higher age, slower resting heart rate before and after atropine and less atropine response during CSP compared to control. Hypersensitivity of the carotid sinus reflex was interpreted as a part of the physiological augmentation of vagal tone in elderly people.