Major hospital complications, including prolonged mechanical ventilation, severe sepsis, and cardiac complications, were more common in patients with SCM (Table 1). The multivariate analysis did not demonstrate a statistically significant association between SCM and vasospasm. Interestingly, among patients with vasospasm, patients with SCM-apical and SCM-basal had a higher use of vasopressors and inotropes (35% and 57%, respectively) compared with patients with no echocardiogram or no RLVD (9% and 13%, respectively, P < 0.0001). Even after adjustment with high-dimensional propensity score, patients with SCM had higher adjusted odds for cardiac complications (OR, 5.3; 99% CI, 2.3–12.3) and severe sepsis (OR, 3.0; 99% CI, 1.2–7.6) compared with patients who did not have an echocardiogram (Table 4). The odds of having cardiac complications (OR, 6.1; 99% CI, 1.8–20.2) and severe sepsis (OR, 5.3; 99% CI, 1.6–17.2) for patients with variant cardiomyopathy-basal form were significantly higher compared with those with no echocardiogram. When analysis was limited only to patients who had an echocardiogram, the adjusted OR for severe sepsis was significantly higher in all patients with SCM (OR, 2.7; 99% CI, 1.04–7.3) and particularly those with cardiomyopathy-basal compared with patients with no RLVD (OR, 4.8; 99% CI, 1.4–16.3; Table 5).
In a single-center cohort, we have demonstrated that 28% of SAH patients undergoing surgical treatment had clinical evidence of cardiac dysfunction requiring evaluation with echocardiography. Among those patients, one-third had SCM with similar distribution of classic, predominately apical RLVD and variant, predominately basal RLVD forms. Our study adds to the evidence that the variant form may be as common as the more frequently reported classic form while confirming the previously reported rates of SCM in SAH patients between 3% and 28%.2,4,9,18,19,36–39 After adjustment with high-dimensional propensity score regression, in spite of the increase in hospital complications and resource utilization, short- and long-term survivals were not different between patients with either SCM form in comparison with patients without RLVD but were lower compared with patients who did not have clinical cardiac dysfunction requiring an echocardiographic evaluation. We observed no difference in cardiovascular-specific mortality rate after discharge. Our finding corroborates recent reports of favorable long-term prognosis for SCM patients with cardiovascular mortality comparable with age- and sex-matched population and recurrence rate of 10% over 4 years.4,6,14,20,21
Even after adjustment with high-dimensional propensity score, the risk of death remained significantly higher in those who had an echocardiogram, regardless of whether the echocardiogram showed normal or abnormal RLVD. Most patients tested with echocardiography had clinical evidence of cardiac dysfunction, manifesting with LV dysfunction, chest pain, electrocardiographic changes, or arrhythmia. The proportion of SAH patients in our cohort requiring echocardiogram for clinically indicated reasons is similar to other cohort reports, ranging from 30% to 44%.9,36,39 This suggests that there were hemodynamic or arrhythmic abnormalities that prompted ordering the echocardiogram that were not captured in our propensity score or available structured electronic clinical data and often are only present in clinical text notes. Alternatively, it is possible that our assessment of RLVD using qualitative assessment of LV segmental wall motion was not sensitive enough to detect clinically relevant ventricular dysfunction that prompted the order for an echocardiogram. The subtle abnormalities of systolic function not appreciated with qualitative assessment that led to clinical instability may have been appreciated with more sophisticated measures. Strain analysis with automated software has identified LV systolic dysfunction despite normal qualitative wall motion and ejection fraction in patients with heart failure.40 In addition, in patients with severe aortic stenosis, quantitative measures of LV longitudinal strain are abnormal, despite a normal ejection fraction.41 Future studies evaluating the use of advanced evaluation of LV systolic function in SAH patients are warranted.
Patients with SCM had significantly increased odds for developing cardiac complications, implying that cardiomyopathy had a functional significance as it has been shown in patients with different causes of SCM.42,43 Severe sepsis was significantly more common in those with SCM even after adjustment for other clinical factors. Although prolonged intubation among SAH patients with SCM has been reported,9 the increased occurrence of severe sepsis is intriguing and may indicate a potential overlap in pathophysiology between the 2 conditions.44 Thus, SCM in SAH patients is associated with higher burden of cardiac and noncardiac complications that may lead to significantly increased resource utilization and hospital cost similar to patients with SCM associated with other conditions.4,14
The prevalence of vasospasm was not different between the patients with SCM and those without RLVD. Previous reports suggest that severe RLVD is a risk factor for delayed cerebral ischemia from vasospasm, but not vasospasm itself.9,38 In SCM patients with low cardiac output, the blood pressure goals for hemodynamic augmentation45 can be difficult to achieve, which is consistent with our finding of increased use of inotropes and vasopressors in patients with SCM and vasospasm. Because catecholamine toxicity is the postulated mechanism for the cardiomyopathy, the administration of catecholamine-based vasopressors and inotropes could worsen the disease process and affect survival.
The retrospective nature of our study limits our evaluation of the functional outcomes of the patients with tools such as Modified Rankin Scale. We used discharge to a rehabilitation center or to home as a surrogate for a moderate disability or less but were unable to demonstrate significance in the negative association between SCM and this outcome. A sample size larger than in our study would be required to further test the recent observation of greater incidence of poor outcome and death in patients with midventricular wall motion abnormalities, a subgroup of basal SCM.19
This was a retrospective cohort; hence, we can neither make the causal inference nor exclude bias from unmeasured factors. The reported prevalence for SCM needs to be interpreted cautiously, because we cannot exclude the possibility of undiagnosed SCM in patients without echocardiogram. We attempted to control for selection bias with multivariable statistical methods and the use of high-dimensional propensity score specifically designed for risk adjustment in claims data34 to offset the potential confounding effect of disease severity and clinical evidence of cardiac dysfunction on the probability of having echocardiogram. Although intriguing, the finding that patients with clinical evidence of cardiac dysfunction had worse outcomes regardless of the echocardiographic findings of SCM needs to be interpreted in the context of small sample size and retrospective study design. Although we assessed comorbidities, sepsis, and cardiac complications using validated approach with ICD-9-CM codes,29,46 the subtle differences in coding definitions may lead to risk underassessment. The inability to observe significant difference, rather than trend, in worse diastolic dysfunction among SCM patients may reflect the small sample size of patients with available diastolic function measurements. Although this is a single-institution report, it comprises a cohort of SAH patients obtained over 10 years with outcomes comparable with that reported in the literature.
Among SAH patients who had an echocardiogram for clinically indicated reasons, variant basal SCM is almost as common as classic apical form. Although we observed no difference in long-term survival among patients with SCM and those without RLVD, patients who had echocardiogram for clinically evident cardiac dysfunction had significantly decreased long-term survival compared with patients with no echocardiogram, even after adjusting for multiple clinical factors with high-dimensional propensity score. This may suggest that clinical events that prompt the order of an echocardiogram, and possibly subtle RLVD that is not detected with qualitative assessments of LV systolic function, have important prognostic implications. The significant association between severe sepsis and SCM warrants future studies to determine whether these complications may augment LV systolic dysfunction among SAH patients.
We thank Gigi Lipori and Yue Du for assistance with data retrieval.
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