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==Overview==
==Overview==
Available data indicate that the development of shock after hospital admission with acute MI is as common as cardiogenic shock on presentation. Because of the > 50% mortality associated with both of these conditions, the most favorable means of making an impact on shock mortality is to prevent its development. Therefore, effective therapy for shock must include a prevention strategy. In the GUSTO study, 70% of patients who developed cardiogenic shock after admission were Killip class I on admission, and of the remaining patients most were in Killip class 11 with only mild heart failure.? For this reason, other clinical clues must be used to recognize patients at high risk for developing shock. The development of tachycardia or evidence ofperiphera1 vasoconstriction are early clinical signs ofthe "preshock" state. Data from the Secondary Prevention Reinfarction Israel Nifedipine Trial (SPRINT) study") suggest that the presence of diabetes, history of angina, peripheral vascular or cerebrovascular disease, prior MI, and female gender are all risks for development of shock in Killip class I patients with acute infarction. These investigators estimated a 35% probability of developing shock if all six of these factors were present on admission. In addition to these clinical factors obtained from the history and physical examination, diagnostic studies such as early two-dimensional echocardiography may be helpful in evaluating selected patients. In a consecutive series of over 80 patients, Gibson etnl. stratified patients with acute MI into two groups: those with asynergy in the infarct zone only and those with asynergy in the infarct zone plus a remote zone. They found that the latter group had a significantly higher incidence of cardiogenic shock (34 vs. 8%, p = 0.01), as well as higher rates of death, reinfarction, and Killip class progression than patients with asynergy in the infarct zone only. It is likely that all of the above information is helpful in identifying patients with triple-vessel coronary artery disease in an otherwise low-risk clinical group (i.e., patients without heart failure on admission).
Available data indicate that the development of shock after hospital admission with acute MI is as common as cardiogenic shock on presentation. Because of the > 50% mortality associated with both of these conditions, the most favorable means of making an impact on shock mortality is to prevent its development. Therefore, effective therapy for shock must include a prevention strategy. In the GUSTO study, 70% of patients who developed cardiogenic shock after admission were Killip class I on admission, and of the remaining patients most were in Killip class II with only mild heart failure. For this reason, other clinical clues must be used to recognize patients at high risk for developing shock. The development of tachycardia or evidence of peripheral vasoconstriction are early clinical signs ofthe "preshock" state. Data from the Secondary Prevention Reinfarction Israel Nifedipine Trial (SPRINT) study") suggest that the presence of diabetes, history of angina, peripheral vascular or cerebrovascular disease, prior MI, and female gender are all risks for development of shock in Killip class I patients with acute infarction. These investigators estimated a 35% probability of developing shock if all six of these factors were present on admission. In addition to these clinical factors obtained from the history and physical examination, diagnostic studies such as early two-dimensional echocardiography may be helpful in evaluating selected patients. In a consecutive series of over 80 patients, Gibson etnl. stratified patients with acute MI into two groups: those with asynergy in the infarct zone only and those with asynergy in the infarct zone plus a remote zone. They found that the latter group had a significantly higher incidence of cardiogenic shock (34 vs. 8%, p = 0.01), as well as higher rates of death, reinfarction, and Killip class progression than patients with asynergy in the infarct zone only. It is likely that all of the above information is helpful in identifying patients with triple-vessel coronary artery disease in an otherwise low-risk clinical group (i.e., patients without heart failure on admission).


==Primary prevention==
==Primary prevention==

Revision as of 23:44, 1 January 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2] Syed Musadiq Ali M.B.B.S.[3]

Overview

Available data indicate that the development of shock after hospital admission with acute MI is as common as cardiogenic shock on presentation. Because of the > 50% mortality associated with both of these conditions, the most favorable means of making an impact on shock mortality is to prevent its development. Therefore, effective therapy for shock must include a prevention strategy. In the GUSTO study, 70% of patients who developed cardiogenic shock after admission were Killip class I on admission, and of the remaining patients most were in Killip class II with only mild heart failure. For this reason, other clinical clues must be used to recognize patients at high risk for developing shock. The development of tachycardia or evidence of peripheral vasoconstriction are early clinical signs ofthe "preshock" state. Data from the Secondary Prevention Reinfarction Israel Nifedipine Trial (SPRINT) study") suggest that the presence of diabetes, history of angina, peripheral vascular or cerebrovascular disease, prior MI, and female gender are all risks for development of shock in Killip class I patients with acute infarction. These investigators estimated a 35% probability of developing shock if all six of these factors were present on admission. In addition to these clinical factors obtained from the history and physical examination, diagnostic studies such as early two-dimensional echocardiography may be helpful in evaluating selected patients. In a consecutive series of over 80 patients, Gibson etnl. stratified patients with acute MI into two groups: those with asynergy in the infarct zone only and those with asynergy in the infarct zone plus a remote zone. They found that the latter group had a significantly higher incidence of cardiogenic shock (34 vs. 8%, p = 0.01), as well as higher rates of death, reinfarction, and Killip class progression than patients with asynergy in the infarct zone only. It is likely that all of the above information is helpful in identifying patients with triple-vessel coronary artery disease in an otherwise low-risk clinical group (i.e., patients without heart failure on admission).

Primary prevention

Attending to the definition of primary prevention, namely the group of measures that aim to avoid the development of a disease state (preventive measures) and considering the fact that left ventricular failure following acute MI is the most common cause of cardiogenic shock, these patients should undergo primary prevention of myocardial infarction.[1]

References

  1. Eckel RH, Jakicic JM, Ard JD, Hubbard VS, de Jesus JM, Lee IM; et al. (2013). "2013 AHA/ACC Guideline on Lifestyle Management to Reduce Cardiovascular Risk: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines". Circulation. doi:10.1161/01.cir.0000437740.48606.d1. PMID 24222015.


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