Cardiogenic Shock - Diagnosis and Treatment

104 Part IV / Mechanical Complications
Risk Factors
Risk factors for VFWR include female gender, advanced age, low body weight, short
stature, strenuous activities during recovery phases, and large myocardial infarct size
(3,58,68,71,72,74–76,81–83) (Table 2). Some studies indicate that women aged 60–69 y
are especially at risk (15,72), although this finding is controversial (3,68). Warning signs
for VFWR may include intraventricular conduction defect on an electrocardiogram (ECG),
echocardiographic signs of lateral wall involvement, and high serum C-reactive proteins
(74,82,84–86). Resuscitation measures, such as external cardiac massage and intracardiac
injections, have also been suggested as possible causes of cardiac rupture (87).
Some factors that are normally considered high risk for serious cardiac diseases may
not be risk factors for cardiac rupture. For example, there are two studies in which
patients who are active smokers are less likely to have a cardiac rupture (75,76),
whereas the study of Pollak et al. reported no difference between smokers and non-
smokers (74). Additionally, in patients with cardiogenic shock, those who develop
VWFR are less likely to have peripheral vascular disease or diabetes mellitus (81).
In patients with hypertension, left ventricular hypertrophy appears to be protective
against cardiac rupture (82,88). Mann and Roberts found the mean heart weights were
lower (although not significantly lower) in patients with hypertension who developed
cardiac rupture (84). Thus, failure to develop left ventricular hypertrophy in response
to hypertension could be a risk factor for VFWR.
A history of hypertension is not considered to be a risk factor for or an independent
predictor of VFWR (3,72,76,84,89). However, some studies show significantly more
hypertension among patients with cardiac rupture than among surviving patients with no
rupture (71,74). VFWR may be associated with acute or sustained hypotension related to
severe heart failure caused by a large infarct (15,72,83). Indeed, Pohjola-Sintonen et al.
found that cardiac rupture was more prevalent in patients with systolic blood pressure
<150 mm Hg than in those with systolic blood pressure >150 mm Hg (3).
Most studies indicate that patients with a history of angina pectoris, prior MI, three-
vessel coronary artery disease, or congestive heart failure are also less likely to develop
VFWR (3,72,74,81,84,90). Prior angina suggests the presence of chronic obstructive
coronary artery disease, which is associated with the development of coronary artery
collaterals that may reduce the incidence of both free wall and septal rupture. In addi-
tion, previous angina may precondition the myocardium and be protective against ven-
tricular septal (20) and free wall rupture. Scar formation resulting from a previous MI
or pericardial thickening resulting from previous inflammation may also offer protec-
tion against VFWR (81,82).
However, there are conflicting data indicating that prior angina, prior MI, or three-
vessel coronary artery disease may not be protective against cardiac rupture. Becker et
al. found prior angina to be an independent risk factor for cardiac rupture (76). In the
National Registry of Myocardial Infarction (NRMI), prior MI was independently asso-
ciated with cardiac rupture (71). Other reports indicate a higher incidence of three-ves-
sel coronary artery disease in patients with cardiac rupture (68,82).
Pathophysiology
Left VFWR usually occurs on the anterior or lateral wall of the left ventricle at the
mid-papillary muscle level (91,92). Veinot et al. found that in 20 of 25 patients (80%),
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