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Lisbon, Portugal
Correspondence to: Boban Thomas, MD, FCCP, Av. Almirante Gago Coutinho, 101, 2 A Dto, 1700–029 Lisbon, Portugal; e-mail: boban_thomas{at}lycos.com
To the Editor:
Dr. Andrew needs to be complimented for chipping away at a myth in the field of heart failure in his enlightening review about diastolic heart failure (August 2003).1 He is right to point out that the tool that has constrained our thinking is the echocardiogram, which has fostered the binary classification of heart failure into either systolic or diastolic. Fortunately, recent data suggest that it may also be the tool that may liberate us from this constrained mode of reasoning.
Yu et al,2 in an elegant study using tissue Doppler echocardiographic imaging, demonstrated the presence and progression of systolic abnormalities in patients classified to have either isolated diastolic heart failure (implying an ejection fraction > 50% for patients who presented with congestive heart failure) or pure diastolic dysfunction. They measured peak myocardial sustained systolic and early diastolic velocities in various myocardial segments after excluding patients with segmental wall motion abnormalities. Systolic and early diastolic velocities correlate well with the rate of tension development and the rate of relaxation determined by cardiac catheterization. Compared with normal control subjects, these parameters were decreased in those with diastolic dysfunction, isolated diastolic heart failure, and systolic heart failure. There was a continuum of worsening of these parameters in the following sequence: normal, diastolic dysfunction, isolated diastolic heart failure, and systolic heart failure.
Therefore, congestive heart failure may actually be a disease of a progressive nature with gradual deterioration of systolic function even though ejection fraction (rightly pointed out to be misleading by the author) determined by echocardiography may seem to remain normal except when the disease has progressed considerably. It is unclear though where those patients classified as asymptomatic systolic left ventricular dysfunction fit into this continuum.
References
Watertown, NY
Correspondence to: Philip Andrew, MD, Watertown Cardiology, 727 Washington St, Watertown, NY 13601; e-mail: philipandrew{at}earthlink.net
To the Editor:
I thank Drs. Munoz and Thomas for their complimentary remarks. Although the important work of Yu et al1 was not cited, I used the term systolic "and/or" diastolic ventricular dysfunction/failure liberally2 to imply the spectrum of systolic/diastolic ventricular dysfunction/failure they described.
I further alluded to the coexistence of systolic dysfunction in diastolic heart failure as: "... an end-systolic volume (ESV) ‘two sizes too big’ to match the low (end-diastolic volume [EDV]) ...", the high ESV "... presumably the result of (1) the inherent mechanical limit to cardiomyocyte shortening, and/or (2) Frank-Starling forces constrained by the constrained EDV."2 In other words, the restricted preload EDV of diastolic dysfunction/failure could itself produce coexisting systolic dysfunction simply by frustrating the Starling mechanism. Supporting such a causal link, Yu et al1 found that systolic dysfunction invariably, globally, and proportionately coexists with diastolic dysfunction.
For all practical purposes the cardiac output (Starling) curve is also the atrioventricular compliance curve. Since all atrioventricles have a compliance limit, all normal and abnormal Starling curves have a near-vertical upper limb (the Starling "wall"2) of near-infinite "diastolic dysfunction" representing this limit. Systolic and/or diastolic dysfunction shifts the Starling wall to the left. EDV at the Starling wall is lower when diastolic dysfunction/failure predominates (although limited unconfirmed anomalous data have appeared34). In any case, in systolic and/or diastolic heart failure the pulmonary venous return (Guyton) curve2 crosses the near-vertical Starling wall common to both, thus anticipating the finding of Yu et al1 that diastolic dysfunction is quantitatively identical in "isolated" diastolic and primarily systolic failure (as peak myocardial sustained early diastolic velocity [EM], Table 4, SHF vs DHF column).
Munoz and Thomas keenly observe that in the continuum of disease progression described by Yu et al1: normal—diastolic dysfunction—"isolated" diastolic failure—systolic heart failure, "asymptomatic systolic dysfunction" is missing as the precursor of systolic heart failure. When EDV is low, as in this group with predominant diastolic dysfunction, the effect of any given superimposed systolic dysfunction/increased ESV on the ejection fraction is mathematically magnified. Thus, even relatively minor increases in ESV are capable of lowering the ejection fraction below 50%, thereby satisfying the definition of systolic heart failure. This might account, at least in part, for the apparent direct transition from "isolated" diastolic failure to systolic heart failure. Also, predominant systolic dysfunction has a compensatory mechanism for preserving stroke volume/"asymptomatic" status that is unavailable in predominant diastolic dysfunction: the ability to increase EDV. Indeed, recent data show that a transition from diastolic to systolic dysfunction over a median period of 50 months occurred in only 
20%. In this subgroup, a baseline history of coronary artery disease was more than twice as likely, and nearly half had a myocardial infarct during the study interval.5
As simplistic and relatively inelegant as the ESV might be as an index of systolic dysfunction, all indices of ventricular dysfunction must nevertheless ultimately affect ESV and/or EDV if cardiac pump function is reduced. The overriding (and still too often disregarded) physiologic significance of ventricular dysfunction is its impact on stroke volume/cardiac output, the primary duty of the heart. Indices of ventricular (tissue) function alone, particularly the ejection fraction, are unreliable indicators of stroke volume. Therefore, they cannot reliably indicate low cardiac output (cardiac function), the cardinal hemodynamic expression of ventricular (tissue) dysfunction and the fundamental abnormality underlying the heart failure syndrome.
References
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