Jacob C. Miss

Acute Neurocardiogenic Injury After Subarachnoid Hemorrhage

Background— Left ventricular (LV) systolic dysfunction has been reported in humans with subarachnoid hemorrhage (SAH), and its underlying pathophysiology remains controversial. Possible mechanisms include myocardial ischemia versus excessive catecholamine release from sympathetic nerve terminals. Methods and Results— For 38 months, echocardiography and myocardial scintigraphy with technetium sestamibi (MIBI) and meta-[123I]iodobenzylguanidine (MIBG) were performed on 42 patients admitted with SAH to assess myocardial perfusion and sympathetic innervation, respectively. A blinded observer interpreted the scintigraphic images. Cardiac troponin I (cTI) was measured to quantify the degree of myocyte necrosis. Blinded observers calculated the LV ejection fraction and graded each LV segment as normal (score=1), hypokinetic (score=2), or akinetic (score=3). A wall-motion score was calculated by averaging the sum of the 16 segments. All subjects with interpretable scans (N=41) had normal MIBI uptake. Twelve subjects had either global (n=9) or regional (n=3) absence of MIBG uptake. In comparison with patients with normal MIBG uptake, those with evidence of functional denervation were more likely to have LV regional wall-motion abnormalities (92% versus 52%, P=0.030) and cTI levels >1 &mgr;g/L (58% versus 21%, P=0.029). Conclusions— LV systolic dysfunction in humans with SAH is associated with normal myocardial perfusion and abnormal sympathetic innervation. These findings may be explained by excessive release of norepinephrine from myocardial sympathetic nerves, which could damage both myocytes and nerve terminals.

Adrenoceptor Polymorphisms and the Risk of Cardiac Injury and Dysfunction After Subarachnoid Hemorrhage

Background and Purpose— Cardiac abnormalities occur commonly after subarachnoid hemorrhage (SAH) and may be caused by excessive release of catecholamines from the myocardial sympathetic nerves. We hypothesized that adrenoceptor polymorphisms resulting in greater catecholamine sensitivity would be associated with an increased risk of cardiac injury. Methods— This was a prospective cohort study. The primary outcome variables were the serum level of cardiac troponin I (cTi, abnormal if >1.0 μg/L) and the left ventricular ejection fraction (LVEF, abnormal if <50%). Six adrenoceptor polymorphisms were genotyped: β1AR Arg389Gly, β1AR Ser49Gly, β2AR Gly16Arg, β2AR Gln27Glu, β2AR Thr164Ile, and α2AR del322-325. The effect of each polymorphism on the risk of developing cardiac abnormalities was quantified using multivariable logistic regression. Results— The study included 182 patients. The CC genotype (Arg/Arg) of β1AR Arg389Gly (odds ratio [OR] 3.4, P=0.030) and the CC genotype (Gln/Gln) of β2AR Gln27Glu (OR 3.1, P=0.032) were predictive of cTi release. The presence of the α2AR deletion was predictive of reduced LVEF (OR 4.2, P=0.023). The combination of the β1AR 389 CC and the β2AR 27 CC genotypes resulted in a marked increase in the odds of cTi release (OR 15.5, P=0.012). The combination of the β1AR 389 CC and the α2AR deletion genotypes resulted in a marked increase in the odds of developing a reduced LVEF (OR 10.3, P=0.033). Conclusions— Genetic polymorphisms of the adrenoceptors are associated with an increased risk of cardiac abnormalities after SAH. These data support the hypothesis that cardiac dysfunction after SAH is a form of neurocardiogenic injury.

Cardiovascular predictors of in-patient mortality after subarachnoid hemorrhage

Background and PurposeWhether cardiac dysfunction contributes to morbidity and mortality after subarachnoid hemorrhage (SAH) remains controversial. The objective of this study was to test the hypothesis that cardiovascular abnormalities are independently related to in-patient mortality after SAH.MethodsThis was a prospective cohort study of patients with aneurysmal SAH. Heart rate and blood pressure were measured, a blood sample was obtained, and echocardiography was performed on three study days, starting as soon after admission as possible. The cardiovascular predictor variables were heart rate, systolic blood pressure (SBP), cardiac troponin I (cTi) level, B-type natriuretic peptide (BNP) level, and left ventricular ejection fraction. The primary outcome measure was in-patient mortality. The association between each predictor variable and mortality was quantified by multivariate logistic regression, including relevant covariates and reporting odds ratios (OR) and 95% confidence intervals (CI).ResultsThe study included 300 patients. An initial BNP level greater than 600 pg/mL was markedly associated with death (OR 37.7, p<0.001). On the third study day (9.1±4.1 days after SAH symptom onset), a cTi level greater than 0.3 mg/L (OR 7.6, p=0.002), a heart rate of 100 bpm or greater (OR 4.9, p=0.009), and a SBP less than 130 mmHg (OR 6.7, p=0.007) were significantly associated with death.ConclusionsCardiovascular abnormalities are independent predictors of in-patient mortality after SAH. Though these effects may be explained by a reduction in cerebral perfusion pressure or other mechanisms, further research is required to determine whether or not they are causal in nature.

Prevalence and implications of diastolic dysfunction after subarachnoid hemorrhage

Introduction: Electrocardiographic changes, troponin release, and reduced left ventricular ejection fraction have been described after subarachnoid hemorrhage (SAH). Little is known about the occurrence of diastolic dysfunction in this setting. The purpose of this study was to determine the prevalence of diastolic dysfunction and its association with cardiac outcomes after SAH.Methods: SAH patients were prospectively enrolled into the study, and echocardiographic, clinical, chest X-ray, and cardiac troponin I data were obtained on days 1, 3, and 6 after enrollment. Each echocardiogram included Doppler recordings of mitral inflow and pulmonary venous flow. For each study, diastolic function was categorized as normal, impaired relaxation, pseudonormal, or restrictive. The relationships between diastolic dysfunction and pulmonary edema-elevated cardiac troponin I and left ventricular contractile dysfunction were quantified using both univariate and multivariate statistical methods. Clinical predictors of diastolic dysfunction were defined by multivariate logistic regression.Results: Of 223 enrolled subjects, 207 had technically adequate Doppler data. Diastolic dysfunction was observed in 71% of subjects. The prevalence of diastolic versus systeolic dysfunction in 44 patients with pulmonary edema was 91 versus 37%, respectively (p=0.001). After multivariate statistical adjustment, diastolic dysfunction remained a significant predictor of pulmonary edema (odds ratio [OR] 3.34, 95% CI=1.05−10.59). Diastolic dysfunction also was associated with troponin release (p=0.02). A history of hypertension and increasing age were predictive of diastolic dysfunction.Conclusion: Diastolic dysfunction is common after SAH. It is associated with history of hypertension and older age and may explain the development of pulmonary edema in many SAH patients.

Cardiac injury after subarachnoid hemorrhage is independent of the type of aneurysm therapy.

OBJECTIVE:Subarachnoid hemorrhage (SAH) is associated with cardiac injury and dysfunction. Whether aneurysm clipping versus coiling has a differential effect on the risk of troponin release and left ventricular (LV) dysfunction after SAH is unknown. It is hypothesized that aneurysm treatment does not affect the risk of developing cardiac injury and dysfunction. METHODS:The study included 172 consecutive SAH patients who underwent clipping (n = 109) or coiling (n = 63) aneurysm therapy. Hemodynamic data were collected, cardiac troponin I was measured, and echocardiography was performed on the 1st, 3rd, and 6th days after enrollment. A cardiac troponin I measurement of more than 1.0 &mgr;g/L was considered abnormal. For each echocardiographic examination, a blinded observer measured LV ejection fraction (abnormal if <50%) and quantified LV regional wall motion abnormalities. The incidence of cardiac outcomes in the treatment groups was compared using odds ratios (ORs). RESULTS:The coiled patients were older than the clipped patients (mean age, 59 ± 13 yr versus 53 ± 12 yr; t test, P < 0.001) and were more likely to have posterior aneurysms (33% versus 18%; &khgr;2 test, P = 0.019). There were no significant between-group differences in the risk of cardiac troponin I release (coil 21% versus clip 19%; OR = 0.89, P = 0.789), regional wall motion abnormalities (33% versus 28%; OR = 0.76, P = 0.422), or LV ejection fraction lower than 50% (16% versus 17%; OR = 1.06, P = 0.892). No patient died of cardiac causes (heart failure, myocardial infarction, or arrhythmia). CONCLUSION:Surgical and endovascular aneurysm therapies were associated with similar risks of cardiac injury and dysfunction after SAH. The presence of neurocardiogenic injury should not affect aneurysm treatment decisions.

Improvised Traction Splints: A Wilderness Medicine Tool or Hindrance?

OBJECTIVES To investigate whether a traction splint made from improvised materials is as efficacious as commercially available devices in terms of traction provided and perceived comfort and stability. METHODS This was a prospective randomized crossover study utilizing 10 healthy, uninjured volunteers. The subjects were randomized to be placed in 4 different traction devices, in differing order, each for 30 minutes. Three of the traction splints are commercially available: The HARE, Sager, and Faretech CT-EMS. The fourth traction device was an improvised splint made as described in Medicine for the Backcountry: A Practical Guide to Wilderness First Aid. At the end of 30 minutes the pounds of force created by each device was measured. The volunteers were also asked at that time to subjectively report the comfort and stability of the splint separately on a scale from 1 to 10. RESULTS All traction splints performed similarly with regard to the primary outcome measure of mean pounds of traction created at the end of 30 minutes of application with results ranging from 10.4 to 13.3 pounds. There was little difference reported by participants in regard to stability or comfort between the 4 traction devices. CONCLUSIONS In this small pilot study, an improvised traction splint was not inferior to commercially available devices. Further research in needed in this area.

Response to Letter by Atanassova

Response: We were interested to read Dr Atanassova’s comments regarding our article. In the design of our study, we excluded patients with a history of myocardial infarction and congestive heart failure (CHF) in order to focus on the pathogenesis of acute cardiac injury and dysfunction. Though subarachnoid hemorrhage (SAH) patients have …

Response to Letter Regarding Article by Banki et al, “Acute Neurocardiogenic Injury After Subarachnoid Hemorrhage”

We were very interested to read Dr Gnecchi-Ruscone’s comments regarding our article.1 Similar to stress cardiomyopathy (SC), elevated catecholamine levels are frequently observed after subarachnoid hemorrhage (SAH).2 In our series, the mean plasma epinephrine and norepinephrine levels were 129±102 pg/mL and 372±494 pg/mL, respectively.3 The majority of the levels are lower than those reported for SC, …