Management of acute cardiogenic shock

The present state of the art in mechanical cardiac assist technology has permitted application of machines to a variety of conditions that confound the cardiologist and cardiac surgeon alike. Decades of research and development have allowed the present devices to be used as bridges to native heart recovery and bridges to transplantation. We are now entering the era in which devices are being placed for permanent assist or replacement. Although the acute cardiogenic shock patient remains problematic, we now have at our disposable a variety of tools that have enabled us to salvage more patients than ever before. The experience with these systems continues to grow, with leading centers and investigators contributing meaningful information toward the application and development of the latest technologies. It has been said that mechanical therapies precede biological therapies. We are at the crossroads in which a combination of biological therapies with mechanical therapies is underway. Current research is investigating the role of mechanical cardiac support while biological therapies are introduced into the failing heart. In the meantime, the role of mechanical cardiac assist and replacement has matured into an effective means of treating acute cardiogenic shock of any variety.     

Cardiogenic shock after acute myocardial infarction

Cardiogenic shock remains the major cause of death among patients with acute myocardial infarction. Besides supportive therapy there is clear evidence that revascularization of the infarct related artery should be performed as soon as possible with percutaneous transluminal coronary angioplasty. Placement of coronary stents and administration of platelet glycoprotein IIb/IIIa antagonists may further improve outcome. Intra-aortic balloon pumping should be integral part of this treatment strategy but is unfortunately underused in clinical practice. Routine bypass surgery for cardiogenic shock patients is deferred and restricted to selected patients.     

Heat shock proteins and acute leukemias

Heat shock proteins (HSPs) acts as molecular chaperones by helping in the refolding of misfolded proteins and assisting in their elimination if they become irreversibly damaged. HSPs induced by stress treatment have a role in the modulation of apoptosis. The reduction in protein expression levels was correlated with an increased susceptibility to drug-induced apoptosis. HSPs have also been implicated in the resistance of leukemia cells to potential therapeutic agents. The mechanisms of cellular protection used by HSPs have yet to be fully defined. HSPs were shown highly expressed by acute myeloid leukemia (AML) cells as well as by acute lymphoblastic leukemia (ALL) cells. HSP expressions were correlated with that of differentiation antigens and that of drug-resistance and apoptosis proteins. Complete remission (CR) rates were higher in patients with lower expression of HSPs. Overall survival (OS) was significantly longer in patients with lower expression of HSPs. Therapeutically, inhibition of inducible HSP expression or activity should not cause any undesired side effects. HSPs emerge as novel therapeutic targets in anticancer protocols. Early results of phase I studies indicate that 17-allylamino-17-demethoxygeldamycin (17-AAG), capable of binding and disrupting the function of HSP90, results in an acceptable toxicity profile while achieving in vivo disruption of multiple oncogenic client proteins.     

Heat shock proteins and acute leukemias

Heat shock proteins (HSPs) acts as molecular chaperones by helping in the refolding of misfolded proteins and assisting in their elimination if they become irreversibly damaged. HSPs induced by stress treatment have a role in the modulation of apoptosis. The reduction in protein expression levels was correlated with an increased susceptibility to drug-induced apoptosis. HSPs have also been implicated in the resistance of leukemia cells to potential therapeutic agents. The mechanisms of cellular protection used by HSPs have yet to be fully defined. HSPs were shown highly expressed by acute myeloid leukemia (AML) cells as well as by acute lymphoblastic leukemia (ALL) cells. HSP expressions were correlated with that of differentiation antigens and that of drug-resistance and apoptosis proteins. Complete remission (CR) rates were higher in patients with lower expression of HSPs. Overall survival (OS) was significantly longer in patients with lower expression of HSPs. Therapeutically, inhibition of inducible HSP expression or activity should not cause any undesired side effects. HSPs emerge as novel therapeutic targets in anticancer protocols. Early results of phase I studies indicate that 17-allylamino-17-demethoxygeldamycin (17-AAG), capable of binding and disrupting the function of HSP90, results in an acceptable toxicity profile while achieving in vivo disruption of multiple oncogenic client proteins.     

Cardiogenic shock complicating acute coronary syndromes

Cardiogenic shock remains the major cause of death among patients with all types of acute coronary syndromes. Thus, there is a growing interest in the identification of patients who are at risk for developing cardiogenic shock, in the exploration of different therapeutic approaches to preventing its development, and in the improvement of outcome when it occurs. This article reviews the aetiology and pathophysiology of cardiogenic shock, its epidemiology, its treatment (including pharmaceutical agents, counterpulsation, and revascularisation), and its outcome. Algorithms are presented that predict its occurrence in both ST-segment-elevation myocardial infarction and unstable angina or non-ST-elevation myocardial infarction, and that predict its mortality in patients with ST-segment-elevation acute myocardial infarction. Such new areas as metabolic therapy and glycoprotein IIb/IIIa inhibitors are discussed, as are the economic implications of shock.     

Cardiogenic shock in acute myocardial infarct patients

To differentiate between various forms of cardiogenic shock (CS) and to elaborate the criteria of its prognosis, the authors examined 284 patients with acute myocardial infarction (MI) and 30 patients of the control group for the peculiarities of the clinical course of the disease in relation to changes in the hemodynamic parameters and oxygen supply to the tissues. CS was shown to develop more frequently in patients over 64 years of age, with a history of MI and with signs of chronic circulation insufficiency of IIA stage. Late CS more commonly took the true form and was associated with a MI relapse. Reflex CS was characterized by the hyperkinetic variant of the hemodynamics while an arrhythmic one by the congestive variant. Patients with the authentic form of CS were divided into 3 subgroups with different hemodynamic reactions to sympathomimetic amines. In the first day of the disease the coefficient of the tissue extraction of oxygen serves as a significant prognostic criterion which should be determined along with the dynamic measurement of the pump and contractile functions of the heart.     

Cardiogenic shock complicating acute myocardial infarction--a review

Cardiogenic shock is characterized by inadequate tissue perfusion due to cardiac dysfunction and is the leading cause of death in patients hospitalized with acute myocardial infarction. Mortality from cardiogenic shock still remains high. The development of cardiogenic shock is rarely unexpected; most patients who develop cardiogenic shock do so within 48 hrs of admission, with only 10% shocked on arrival. Mortality rate is exceedingly high and reaches 70-80% in those treated conservatively. Early revascularization is the cornerstone treatment of acute myocardial infarction complicated by cardiogenic shock. According to the guidelines, revascularization is effective up to 36 hours after the onset of cardiogenic shock and performed within 18 hours after the diagnosis of cardiogenic shock. Primary percutaneous coronary intervention is the most efficient therapy to restore coronary flow in the infarct-related artery. However, invasive strategy in a developing country like ours is not only costly but also technically demanding. We present a case of acute myocardial infarction complicated with cardiogenic shock that underwent primary percutaneous coronary intervention and also review the incidence, pathophysiology, management and outcome of cardiogenic shock complicating acute myocardial infarction.     

Prenalterol in cardiogenic shock following acute myocardial infarction

Eleven patients with cardiogenic shock following acute myocardial infarction (AMI) have been treated with prenalterol. This drug was administered in seven patients once dobutamine or dopamine proved to be ineffective or poorly effective, and it was the first inotropic drug employed in four patients. Therapeutic dose of intravenous infusion ranged from 2.2 to 18 μg/kg/min (mean dose: 7 μg/kg/min), and was maintained for 2 to 4 hours. Since two patients received the infusion on two different occasions, a total of 13 cases were considered for statistical analysis. Prenalterol produced an increase in cardiac index (p < 0.01), mean aortic pressure (p < 0.02), net work index (p < 0.01), net/stroke work index (p < 0.01), pressure rate product (p < 0.05), and myocardial perfusion gradient (p < 0.02). It decreased systemic (p < 0.02) and pulmonary (p < 0.01) vascular resistances, pulmonary artery (p < 0.01) and pulmonary capillary (p < 0.05) pressures. Heart rate and right atrial pressure were not significantly changed. The drug acted as a relatively selective inotropic agent without a chronotropic effect and with minimal peripheral actions. It was effective in seven patients and ineffective in four patients. Thus prenalterol appears to be a useful drug in cardiogenic shock and further studies are warranted.     

A cold shock response triggering acute myocardial infarction

Acute risk factors are activities and events that suddenly and transiently increase the risk of acute cardiac events, as reported recently in International Journal of Cardiology. It has already been reported that sudden submersion in cold water may provoke myocardial infarction in both subjects with atherosclerotic coronary disease and young people with angiographically normal coronary arteries.We report a case of an acute myocardial infarction triggered by sudden exposure to cold air temperature extreme in a young person with acutely occluded proximal part of the left anterior descending coronary artery and normal other coronary arteries who had extreme obesity and cigarette smoking as cardiovascular risk factors.Our report indicates that the sudden cold exposure and the resulting cold shock response may provoke acute myocardial infarction in young susceptible patients.     

Cardiogenic shock due to acute myocarditis complicating leptospirosis

A 48 year old man was admitted to the intensive care unit with septicaemic shock associated with febrile jaundice and anuric renal failure. Within hours, he developed cardiogenic shock with multi-organ failure due to an acute myocarditis refractory to catecholamines and requiring intra-aortic balloon pumping. The diagnosis was an ictero-haemorrhagic leptospirosis, the outcome of which was finally favourable. Myocarditis is an underestimated complication of leptospirosis because it is often symptomless. The main signs are arrhythmias, conduction defects and ST-T wave abnormalities which have little clinical expression. The disease may progress and is sometimes fatal. Leptospirosis myocarditis should therefore be carefully considered because of its potential severity and its reversibility with appropriate antibiotic therapy and also the necessity of initial management in a specific infrastructure.