doi: 10.1161/CIRCULATIONAHA.106.628255
(Circulation. 2006;114:e14.)
© 2006 American Heart Association, Inc.
Correspondence |
Response to Letter Regarding Article "Contractile Behavior of the Left Ventricle in Diastolic Heart Failure: With Emphasis on Regional Systolic Function"
Division of Cardiology, Department of Medicine, University of Massachusetts Medical School, Worcester, Mass
Division of Cardiology, Department of Medicine, Medical University of South Carolina, Charleston, SC
Department of Cardiovascular Medicine, Lahey Clinic, Burlington, Mass
We appreciate Dr Sanderson’s interest and support of our efforts to better understand cardiac function in patients with diastolic heart failure (DHF) and welcome the opportunity to respond. We have previously reported normal left ventricular systolic performance, function, and contractility in patients with DHF and have concluded that the pumping ability of the whole ventricle is normal in the basal state.1 To our knowledge, there are no published data that refute this position. Dr. Sanderson suggests that annular (etc) velocities are of "some significance" and concedes they are "normal in some patients." In fact, as is apparent from a review of our Table 2, these indices are normal in most patients with DHF.2 Such disturbances in regional function have long been recognized, but there is no evidence that reduced midwall strain or tissue Doppler imaging long-axis systolic velocities contribute to, let alone cause, heart failure when all indices of global systolic pump function are normal. We hope that Dr Sanderson would agree with the fact that long-axis function is abnormal in only "some" DHF patients, and this constitutes important evidence that long-axis dysfunction does not cause DHF. Moreover, there are data from our group3 and other investigators to support the position that regional LV dysfunction is present in as many as one third of individuals with hypertensive left ventricular remodeling who do not have heart failure.
Dr Sanderson is correct that long-axis shortening has not been measured in DHF on admission. This appears to be an opportunity for research into the mechanism of acute heart failure. However, left ventricular global systolic function at the time of admission has been shown to be normal by our group and at least 2 others4–5 and appears to change little between short-term and convalescent echocardiography.
We believe that the exciting development of new imaging technologies will enable us to better understand cardiac function, particularly in DHF and asymptomatic hypertensive heart disease. Furthermore, we hope that investigators using these technologies will recognize the need to properly normalize their measurements,2 one of our principal messages. Finally, we agree with Dr Sanderson that it surely "time to move on"—to conclusions based on data, not speculation.
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Acknowledgments |
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Disclosures
None.
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References |
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 Top References |
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1. Baicu CF, Zile MR, Aurigemma GP, Gaasch WH. Left ventricular systolic performance, function, and contractility in patients with diastolic heart failure. Circulation. 2005; 111: 2306–2312.
2. Aurigemma GP, Zile MR, Gaasch WH. Contractile behavior of the left ventricle in diastolic heart failure: with emphasis on regional systolic function. Circulation. 2006; 113: 296–304.
3. Aurigemma GP, Silver KH, Priest MA, Gaasch WH. Geometric changes allow for normal ejection fraction despite depressed myocardial shortening in hypertensive left ventricular hypertrophy. J Coll Cardiol. 1995; 26: 195–202.[CrossRef]
4. Gandhi SK, Powers JC, Nomeir AM, Fowle K, Kitzman DW, Rankin KM, Little WC. The pathogenesis of acute pulmonary edema associated with hypertension. N Engl J Med. 2001; 344: 17–22.
5. Bogaty P, Mure P, Dumesnil JG. New insights into diastolic dysfunction as the cause of acute left-sided heart failure associated with systemic hypertension and/or coronary artery disease. Am J Cardiol. 2002; 89: 341–345.[CrossRef][Medline] [Order article via Infotrieve]
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