Lack of Inertia Force of Late Systolic Aortic Flow Is a Cause of Left Ventricular Isolated Diastolic Dysfunction in Patients With Coronary Artery Disease
Takayuki Yoshida, MD,
Nobuyuki Ohte, MD, FACC*,
Hitomi Narita, MD,
Seiichiro Sakata, MD,
Kazuaki Wakami, MD,
Kaoru Asada, MD,
Hiromichi Miyabe, MD,
Tomoaki Saeki, MD and
Genjiro Kimura, MD
Department of Internal Medicine and Pathophysiology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan
View larger version (13K):
[in a new window]
|
Figure 1 A flow diagram of patients' classification. (A) Patients' classification from the viewpoint of baseline disease. (B) Patients' classification from the standpoint of left ventricular function. CAD = coronary artery disease; Combined MI = anterior myocardial infarction plus inferior MI; LVEF = left ventricular ejection fraction.
|
|
View larger version (13K):
[in a new window]
|
Figure 2 Left ventricular pressure (LVP)–first derivative of left ventricular pressure (dP/dt) relationship (phase loop). (A) A loop obtained from a patient with inertia force. (B) A loop obtained from a patient without inertia force. The negative inverse slope of the best linear-fitting line between the points a and b is equal to the time constant of exponential pressure decay during isovolumic relaxation (Tp). The Tp was 56.3 ms in A and 83.1 ms in B. The area in red divided by the vertical distance between P0,0 and point d is equal to the amount of pressure decay augmented by the effect of the inertia of blood flowing out of the LV, and is defined as the inertia force. The inertia force in A was 3.6 mm Hg, and 0.12 mm Hg in B.
|
|
View larger version (12K):
[in a new window]
|
Figure 3 Relationships between inertia force and left ventricular (LV) systolic function parameters. (A) Relation of inertia force to LV ejection fraction (LVEF). A significant positive correlation is observed. (B) Relation of inertia force to LV end-systolic volume index (ESVI). A significant inverse correlation is found. Circles = patients with preserved systolic function with inertia force; squares = patients with preserved systolic function without inertia force; X = patients with systolic dysfunction.
|
|
View larger version (11K):
[in a new window]
|
Figure 4 Relationships between inertia force and parameters of left ventricular relaxation (Tp) and left ventricular early diastolic filling (Vp). A Relation of inertia force to Tp. A significant inverse correlation is observed. B Relation of inertia force to Vp. A significant positive correlation is found. Symbols are as in Figure 3; other abbreviations as in Figure 1.
|
|
View larger version (20K):
[in a new window]
|
Figure 6 Comparisons of the mitral annular velocity during early diastole (Em) and the propagation velocity of left ventricular early diastolic flow (Vp) between the patient groups. (A) Em was significantly lower both in patients with SDF and in those with PSF without inertia force than in those with PSF with inertia force. (B) Vp was also significantly less in the first 2 groups than in the last group. *p < 0.001;  p < 0.05. Other abbreviations as in Figure 5.
|
|
View larger version (19K):
[in a new window]
|
Figure 7 Comparisons of left ventricular systolic function parameters between patients with PSF with inertia force and those with PSF without inertia force. (A) Left ventricular ESVI was significantly smaller in patients with PSF with inertia force than in those with PSF without inertia force. (B) Left ventricular ejection fraction (LVEF) was significantly greater in the former than in the latter. (C) Peak mitral annular velocity during systole (Sm) was also significantly greater in the former than in the latter. *p < 0.001; p < 0.05. Other abbreviations as Figures 3 and 5.
|
|
View larger version (33K):
[in a new window]
|
Figure 8 Schematic diagram demonstrating the concept that inertia force of late systolic aortic flow enhances left ventricular (LV) elastic recoil. (A) Left ventricles with relatively better LV systolic function give inertia to the late systolic aortic flow. In late systole, when LV muscle shortening has reached a limit but its tension-bearing ability is still maintained, the inertia of the blood flowing out of the LV causes swift end-systolic unloading of the LV, producing additional LV muscle shortening and hence smaller LV end-systolic volume. The resulting greater elastic recoil force brings faster LV relaxation. (B) Left ventricles with impaired contractile function do not give inertia to the late systolic aortic flow. Hence, the swift LV end-systolic unloading caused by the inertia force does not occur. LV relaxation is slow because of the lack of LV elastic recoil.
|
|
|
p < 0.01;