Methods

We retrospectively reviewed medical records of all patients with post-AMI VSR or acute MR who were treated at our center from January 1997 to February 2013. For further analysis, we included only patients in cardiogenic shock or hemodynamically unstable patients who did not fulfill the criteria of shock. Shock was defined as persistent systolic blood pressure of <90 mm Hg (or a decrease in mean arterial pressure of >30 mm Hg), accompanied by pulmonary congestion and/or reduced organ perfusion (cool extremities, altered mental status, oliguria, or acidosis). Patients with systolic blood pressure from 90 to 110 mm Hg on vasopressors or inotropes and radiologic evidence of pulmonary congestion were classified as nonshock (unstable) group.

All patients were admitted to a specialized intensive care unit and managed in a close collaboration with cardiothoracic surgeons. In line with existing guidelines, all operable patients were referred for surgical correction. Pending the surgery, the patients usually received IABP to improve hemodynamics (Datascope IABP—models 98, cs100, and cs300, respectively; Maquet, Solna, Sweden). Decision to use IABP in the patients without shock was based mainly on the magnitude of the shunt or regurgitation and the patient’s general condition. Eight patients in shock did not receive IABP for the following reasons: consensus decision for conservative treatment because of advanced age and major co-morbidities (n = 3), severe iliac arteries tortuosity (n = 2), temporary hemodynamic improvement with medical treatment (n = 2), and need of immediate surgery for cardiac tamponade (n = 1).

Data are summarized as mean ± SD, median and interquartile range, or frequency and percentage. Variables of interest were compared between VSR and MR groups and shock and nonshock patient groups. Continuous variables were compared by Student t or Mann-Whitney test; categorical variables were compared by chi-square or Fisher’s exact test. Kaplan-Meier and Cox proportional hazard regression analyses were performed to determine predictors of survival at 30 days from manifestation of the mechanical complication. All analyses were performed in SPSS 16.0 (SPSS Inc., Chicago, Illinois). p Value at <0.05 was considered significant.

Results

We observed post-AMI VSR in 63 patients (1 to 7 cases/year) and acute severe MR in another 26 patients (0 to 4 cases/year). From further analysis, we excluded 8 asymptomatic patients with an incidental finding of a small VSR. In the rest of the population, the defects manifested with either cardiogenic shock (n = 46) or hemodynamic instability (n = 35). Table 1 lists the general characteristics of the study population.

Both types of post-AMI mechanical complications developed on average on the third day after index infarction (range, 1 to 20 days). Location of the VSR in the septum matched the site of myocardial infarction (anteroapical vs inferobasal, 56% vs 44%). Acute MR occurred almost invariably after inferior wall infarction due to dysfunction or rupture of the posteromedial papillary muscle (proportion of posteromedial vs anterolateral papillary muscle was 93% vs 7%). Although the patients with acute MR compared with those with VSR were on average younger and presented with higher left ventricular ejection fraction, regurgitation led more often to rapid progression of cardiogenic shock, pulmonary edema requiring mechanical ventilation, and, consequently, to faster referral for surgery. However, despite more acute clinical presentation, outcomes of the patients with MR did not differ from those with VSR ( Table 1 ).

IABP was inserted in 38 (83%) of the patients with shock and 20 (57%) of the unstable patients without shock to achieve hemodynamic stability until surgical intervention. All but 3 patients received IABP within the first 24 hours of the hemodynamic deterioration (range, 0 to 4 days). It was removed shortly afterward in 2 of the patients (3%) because of severe limb ischemia. No other IABP-related complications occurred. All 8 patients who did not receive IABP support died within the subsequent 1 to 3 days. The use of IABP support for shock was associated with reduced preoperative mortality (11% vs 88%, p <0.001), which in turn translated into reduced 30-day mortality (61% vs 100%, p = 0.040; see Table 2 and Figure 1 ). Contrary, all the patients without shock survived until the operation, regardless of the presence or absence of IABP support. In other words, the use of IABP did not reduce preoperative and, consequently, 30-day mortality (20% vs 27%, p = 0.7) in the patients without shock (see Table 2 and Figure 1 ).

Kaplan-Meier plot showing the effect of IABP support on 30-day survival in patients with cardiogenic shock and unstable patients without shock with post–myocardial infarction VSR or acute severe MR. Data are linearly interpolated for better clarity.

Seventy patients (86%) survived until surgical repair of the defect. Additional coronary artery bypass grafting was performed in 71% of the procedures. Correction of MR was performed using mitral valve replacement (n = 18) and, less frequently, by papillary muscle repair (n = 4). Patients with shock underwent surgical intervention within a median of 1 day (1 to 2) from onset of the mechanical complication, whereas in the patients without hock, the operation was postponed for a median of 9 days (2 to 18; p <0.001). Shorter time from onset of myocardial infarction to the surgery was associated with better survival of patients with shock ( Table 2 ). None of the patients with MR had significant postoperative regurgitation or paraprosthetic leak. In contrast, 11 (23%) of the patients operated for VSR had residual left-to-right shunt or recurrent rupture of the tissue, for which 4 underwent reoperation. The presence of residual shunt was not related to preoperative hemodynamic status, the use of IABP, or delay to surgery. The residual shunt also did not affect 30-day mortality.

Perioperative mortality reached 40%. Two patients (3%) died during the procedure, another 7 (10%) died within <24 hours, and another 19 (27%) died within a median of 3 days (1 to 8) after the operation. Mechanisms of death included circulatory failure (n = 18), multiorgan failure (n = 4), acute respiratory distress syndrome (n = 4), and tamponade (n = 2). Perioperative mortality was associated with reduced left ventricular ejection fraction (42 ± 11% vs 48 ± 11%, p = 0.046), greater number of significantly stenosed coronary arteries (1.8 ± 0.6 vs 1.4 ± 0.6, p = 0.006), and presence of cardiogenic shock (44% vs 23%, p = 0.053), but it was not related to surgical timing.

The patients were followed for a median of 7 years (2 to 11). Overall 30-day and long-term mortalities (including pre-, peri-, and postoperative mortalities) reached 38% and 62%, respectively. Mortality at 30 days from onset of the mechanical complication was associated with the presence of shock (67% vs 23%, p <0.001), reduced left ventricular ejection fraction (42 ± 10% vs 50 ± 11%, p = 0.002), need for mechanical ventilation with endotracheal intubation (67% vs 37%, p = 0.001), and absence of surgical intervention (100% vs 40%, p <0.001). In Cox proportional hazard models, only the preoperative shock and unperformed surgery were independent predictors of 30-day mortality (hazard ratio 3.4, 95% confidence interval 1.5 to 8 and hazard ratio 5.1, 95% confidence interval 2.2 to 11, respectively; p = 0.004 and p <0.001, respectively). Similar associations were found with respect to all-cause long-term mortality.