Cardiogenic Shock: A Summary of the Randomized SHOCK Trial

Venu Menon, MD, Rupert Fincke, MD


CHF. 2003;9(1) 

In This Article

Etiology of Shock

The etiology of shock was aggressively pursued in the SHOCK trial and registry. While the trial enrolled patients with predominant LV failure, other causes of CS were included in the registry[10] (predominant LV failure, 74.3%; acute, severe mitral regurgitation, 8.3%; ventricular septal rupture, 4.6%; "isolated" right ventricular shock, 3.4%; tamponade rupture, 1.7%; other, 8%). Contrary to classical teaching, mechanical complications occurred early post-MI and the median time from MI to interventricular septal rupture (VSR) in this setting was 16 hours.[11] Reasons for this discrepancy deserve mention. Classical teaching was largely based on surgical series that reported mainly on rupture patients surviving to the operating room.[12,13] Further, the mean time to VSR was frequently used. As VSR can occur both early and late post-MI, the true timing may have been misrepresented in these skewed observations. Overall outcome for patients with diagnosed VSR in the setting of CS was dismal: of the 55 patients registered, only seven survived. Thirty-one patients underwent ventricular septal repair, but only six survived. Consequently, all patients with VSR complicating acute MI should be immediately referred for surgery. The onset of hemodynamic instability in this population is unpredictable and associated with a poor prognosis.

By virtue of infarct size, CS is more common after anterior MI (60% in SHOCK).[7] However, a sizable minority of subjects enrolled in the SHOCK trial had an index inferior wall MI. In the SHOCK registry, more than one third of patients with inferior MI had either a prior MI or a mechanical cause of shock.[10] Patients with inferior MI and CS need to be carefully evaluated. An early screening echocardiogram in this group appears to be of great clinical utility. The echo image quantifies the area of LV infarction and the compensatory response of the remote myocardium. It confirms the integrity of cardiac anatomy by screening for ventricular or free wall rupture, tamponade, and papillary muscle rupture, all of which necessitate emergent surgery. Finally, the functional status of the right ventricle can be evaluated. In the setting of severe right-sided dysfunction, iatrogenic fluid overload may cause a significant septal shift, impair LV filling, and cause right-to-left shunting via a patent foramen ovale.

Subjects presenting with CS have left main (20% in SHOCK) or triple-vessel disease (64%) and severely reduced LV function on cardiac catheterization (mean ejection fraction, 31%).[7] This is in contrast to the preserved LV function (mean ejection fraction, 58%±15% on 90-minute ventriculograph in GUSTO-1)[14] and single-vessel disease (52% in GUSTO-1) seen with the universe of ST elevation MI.[15] Consequently, any revascularization strategy in the setting of CS must include provisions for emergent coronary artery bypass surgery. An isolated percutaneous intervention approach will be hampered by the limited success with unprotected left main stenting as well as multivessel angioplasty in this critical setting. Limited expertise also limits the performance of multivessel angioplasty under percutaneous bypass.[16] A strategy of percutaneous transluminal coronary angioplasty (PTCA) of the infarct related artery followed by coronary artery bypass grafting (CABG) may be useful in certain anatomic subsets but remains formally untested.


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