Correspondence
Diastolic Dysfunction and Hypertension
N Engl J Med 2001; 344:1401-1402May 3, 2001
- Article
To the Editor:
Gandhi et al. (Jan. 4 issue)1 may well be correct in their conclusion that diastolic dysfunction is the primary cause of pulmonary edema in hypertensive heart failure, but the left ventricular ejection fraction is probably inadequate as the sole measure of global systolic function on the basis of which to exclude the possible role of systolic dysfunction. The ejection fraction is recognized to be a relatively crude measure of left ventricular systolic function. Assessment of the ventricular long-axis excursion or velocity by Doppler imaging of the tissue may be a more sensitive index of ventricular function.2 The longitudinal fibers in the myocardium lie in the subendocardium and are therefore especially prone to ischemia, which may be insufficient to produce an obvious regional wall-motion abnormality or an obvious change in the ejection fraction.
Recently, in a group of patients with diastolic heart failure, it was found that both systolic excursion and systolic velocity were significantly reduced in patients with diastolic heart failure, as compared with those in an age-matched group of normal subjects, although the left ventricular ejection fraction was within the normal range.3 It appeared that the patients with diastolic heart failure were an intermediate group between subjects with normal cardiac function and those with obviously depressed systolic function and heart failure. Thus, systolic function may not be truly normal in this group of patients; rather, there may be more subtle changes in ventricular systolic function that affect diastole and that cannot be detected by the measurement of the ejection fraction.
3 ReferencesGabriel W.K. Yip, M.R.C.P.
John E. Sanderson, M.D., F.R.C.P.
Chinese University of Hong Kong, Hong Kong, China1
Gandhi SK ,Powers JC ,Nomeir A-M , et al. The pathogenesis of acute pulmonary edema associated with hypertension. N Engl J Med 2001;344:17-22
Full Text | Web of Science | Medline2
Henein MY ,Gibson DG . Long axis function in disease. Heart 1999;81:229-231
Web of Science | Medline3
Yip GWK ,Wang M ,Ho PY ,Sanderson JE . Left ventricular long axis in diastolic heart failure: is left ventricular function truly normal? Eur J Echocardiogr 2000;2:Suppl 2:S60-S60
To the Editor:
Gandhi et al. showed that the occurrence of acute pulmonary edema in patients with marked hypertension was due to the isolated, transient exacerbation of diastolic dysfunction. In their discussion, the authors rule out the occurrence of systolic dysfunction or mitral regurgitation as a cause of the pulmonary edema, but they do not explicitly identify the mechanism underlying diastolic dysfunction. Hypertension results in an increase in afterload on the left ventricle. It is well known that, in contrast to a limited elevation of afterload,1 a substantial increase in afterload slows myocardial relaxation to such an extent that it induces an upward shift in the end-diastolic pressure–volume relation even in healthy hearts.2 The resulting diastolic dysfunction is due to the lack of sufficient time for the ventricle to relax completely.3 This mechanism might help to explain the results of Gandhi et al.: the delay in relaxation of the ventricle might exacerbate the diastolic dysfunction and congestion caused by severe hypertension. Such a mechanism is even more likely to be present in patients who have alterations in diastolic function when their blood pressure is normal, as evidenced by the pseudo-normal, if not still restrictive, mitral-inflow signals after treatment. We suggest that there is an alternative meaning for the title of the editorial that accompanied the report of Gandhi et al.: “Diastolic Heart Failure — No Time to Relax.”4
4 ReferencesAdelino F. Leite-Moreira, M.D., Ph.D.
Jorge Correia-Pinto, M.D.
University of Porto, 4200-319 Porto, PortugalThierry C. Gillebert, M.D., Ph.D.
University of Antwerp, B2650 Edegem, Belgium1
Leite-Moreira AF ,Gillebert TC . Nonuniform course of left ventricular pressure fall and its regulation by load and contractile state. Circulation 1994;90:2481-2491
Web of Science | Medline2
Leite-Moreira AF ,Correia-Pinto J ,Gillebert TC . Afterload induced changes in myocardial relaxation: a mechanism for diastolic dysfunction. Cardiovasc Res 1999;43:344-353
CrossRef | Web of Science | Medline3
Leite-Moreira AF ,Correia-Pinto J . Load as an acute determinant of end-diastolic pressure-volume relation. Am J Physiol Heart Circ Physiol 2001;280:H51-H59
Web of Science | Medline4
Vasan RS ,Benjamin EJ . Diastolic heart failure -- no time to relax. N Engl J Med 2001;344:56-59
Full Text | Web of Science | Medline
To the Editor:
Gandhi et al. studied hypertensive patients who presented with acute pulmonary edema and noted that there was preserved left ventricular systolic function, which did not change substantially after the resolution of the symptoms. The authors infer that diastolic dysfunction was the cause of pulmonary edema. The only other possibilities they entertain are pulmonary disease and transient severe mitral regurgitation. An important underlying cause of transient pulmonary edema in hypertensive patients is renal-artery stenosis, especially in patients with bilateral disease or severe stenosis in a solitary functioning kidney.1 Pulmonary edema usually resolves after diuresis, as was the case with patients included in the study by Gandhi et al. In patients who have recurrent pulmonary edema with renal-artery disease, resolution after successful percutaneous renal-artery revascularization has been reported.2 This treatable cause of acute pulmonary edema should be considered in hypertensive patients with normal or nearly normal left ventricular systolic function.
2 ReferencesG. Muqtada Chaudhry, M.D.
Robert M. Schainfeld, M.D.
St. Elizabeth's Medical Center, Boston, MA 021351
Missouris CG ,Buckenham T ,Vallance PJ ,MacGregor GA . Renal artery stenosis masquerading as congestive heart failure. Lancet 1993;341:1521-1522
CrossRef | Web of Science | Medline2
Rajachandran M ,Schainfeld R ,Chaudhry GM ,Pieczek A ,Haley L ,Rosenfield K . Episodic pulmonary edema in association with renal artery stenosis: successful treatment by percutaneous renal artery revascularization. J Am Coll Cardiol 1997;29:486A-486A
CrossRef
Author/Editor Response
The authors reply:
To the Editor: We agree with Drs. Yip and Sanderson that patients with a normal ejection fraction and diastolic dysfunction may have subtle abnormalities of left ventricular contraction. The ejection fraction (the stroke volume divided by the end-diastolic volume) is an integrated measure of left ventricular systolic performance. Thus, it can remain in the normal range despite a mild depression of myocardial contraction.1 Our finding that there was no decrease in the ejection fraction during acute hypertensive pulmonary edema indicates that any transient myocardial dysfunction that was present was not sufficient to depress left ventricular ejection. Although many of the patients in our study who had normal ejection fractions may have had subtle abnormalities of myocardial contraction, a transient decrease in systolic function was not the cause of the hypertensive pulmonary edema.
Elegant studies by Leite-Moreira et al. have demonstrated that marked increases in the systolic load increase the left ventricular diastolic pressure and slow left ventricular relaxation.2 This mechanism contributes to the diastolic dysfunction in patients with hypertensive pulmonary edema. The left ventricle compensates for an acute increase in afterload by using preload reserve. If the left ventricular distensibility is reduced because of preexisting diastolic dysfunction or the effects of markedly elevated systolic pressure, there will also be a marked increase in left atrial pressure. Although slowed relaxation has a role, we doubt that it is the only mechanism contributing to the development of pulmonary edema.3
Drs. Chaudhry and Schainfeld emphasize the important point that hypertensive pulmonary edema can occur in patients with bilateral renal-artery stenosis. Although renal-artery stenting is a potentially attractive therapy, its role in preventing recurrent pulmonary edema has not been defined.
3 ReferencesSanjay K. Gandhi, M.D.
John C. Powers, M.D.
William C. Little, M.D.
Wake Forest University School of Medicine, Winston-Salem, NC 27157-10531
Little WC. Assessment of normal and abnormal cardiac function. In: Braunwald E, Zipes DP, Libby P, eds. Heart disease: a textbook of cardiovascular medicine. Vol. 1. 6th ed. Philadelphia: W.B. Saunders, 2001:479-502.
2
Leite-Moreira AF ,Correia-Pinto J ,Gillebert TC . Afterload induced changes in myocardial relaxation: a mechanism for diastolic dysfunction. Cardiovasc Res 1999;43:344-353
CrossRef | Web of Science | Medline3
Little WC . Enhanced load dependence of relaxation in heart failure: clinical implications. Circulation 1992;85:2326-2328
Web of Science | Medline
Author/Editor Response
The editorialists reply:
To the Editor: We thank Leite-Moreira et al. for drawing attention to the intended double meaning of the title of our editorial, “Diastolic Heart Failure — No Time to Relax.” Diastolic heart failure is characterized by the inability of the left ventricle to relax effectively during the time of diastole. The clinical and scientific communities' approach to diastolic heart failure has been characterized by an incomplete implementation of the primary preventive therapy that is known to be efficacious (treating hypertension), the lack of a gold standard for the diagnosis of the condition, and a paucity of evidence-based strategies to guide therapy. Hence, our message, reflected in the title, was that it is not time for the clinical and research communities to relax in seeking a solution to the fundamental problem of impaired left ventricular relaxation.
Ramachandran S. Vasan, M.D.
Framingham Heart Study, Framingham, MA 01702Emelia J. Benjamin, M.D.
Boston University School of Medicine, Boston, MA 02118
