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Stroke. 2006;37:2873
Published online before print October 12, 2006, doi: 10.1161/01.STR.0000248200.15086.97
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(Stroke. 2006;37:2873.)
© 2006 American Heart Association, Inc.


Letters to the Editor

Response to Letter by Atanassova

Jonathan G. Zaroff, MD; Ludmila Pawlikowska, PhD; Jacob C. Miss, BA; Sirisha Yarlagadda, MD; Connie Ha, BS; Achal Achrol, BS; Pui-Yan Kwok, MD, PhD; Charles E. McCulloch, PhD; Michael T. Lawton, MD; Nerissa Ko, MD; Wade Smith, MD, PhD William L. Young, MD

University of California San Francisco Medical Center, San Francisco, Calif

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 prevalent hypertension and smoking, the majority of patients are women, the mean age is <60 years, and the prevalence of diabetes mellitus and dyslipidemia is low. These factors likely limit the prevalence of overt or occult coronary artery disease (CAD) and CHF in this population. In screening for a total cohort size of 300 patients, <10 patients were excluded because of a history of prior myocardial infarction or CHF.

Though it is impossible to precisely predefine the cardiac status of all victims of sudden events such as SAH, the available data indicate that cardiac enzyme,1 echocardiographic,2 and electrocardiographic3 abnormalities normalize over time, which would not be expected if the abnormalities preceded the SAH.

In our multivariate models predicting troponin release and left ventricular systolic dysfunction, we did adjust for Hunt&Hess grade, a reasonable surrogate for initial neurological status. We did not adjust for hypertension or pre-existing CAD in order to preserve the statistical power of the models, given the limited sample size. In addition, in other analyses of this dataset, we have shown that CAD and coronary risk factors, including hypertension, smoking, diabetes mellitus, and dyslipidemia, are not predictive of troponin release1 or left ventricular systolic dysfunction.4

Acknowledgments

Disclosures

None.

References

  1. Tung P, Kopelnik A, Banki N, Ong K, Ko N, Lawton MT, Gress D, Drew B, Foster E, Parmley WW, Zaroff J. Predictors of neurocardiogenic injury after subarachnoid hemorrhage. Stroke. 2004; 35: 548–551.[Abstract/Free Full Text]
  2. Banki N, Kopelnik A, Tung P, Lawton MT, Gress D, Drew B, Dae M, Foster E, Parmley W, Zaroff J. Prospective analysis of prevalence, distribution, and rate of recovery of left ventricular systolic dysfunction in patients with subarachnoid hemorrhage. J Neurosurg. 2006; 105: 15–20.[Medline] [Order article via Infotrieve]
  3. Sommargren CE. Electrocardiographic abnormalities in patients with subarachnoid hemorrhage. Am J Crit Care. 2002; 11: 48–56.[Abstract/Free Full Text]
  4. Kothavale A, Banki NM, Kopelnik A, Yarlagadda S, Lawton MT, Ko N, Smith WS, Drew B, Foster E, Zaroff JG. Predictors of left ventricular regional wall motion abnormalities after subarachnoid hemorrhage. Neurocrit Care. 2006; 4: 199–205.[CrossRef][Medline] [Order article via Infotrieve]

Related Article:

Previous Cardiac Abnormalities in Subarachnoid Hemorrhage May Also Have Background Genetic Polymorphisms
Penka A. Atanassova
Stroke 2006 37: 2872. [Full Text] [PDF]




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