Effect of medical therapy for heart failure on segmental myocardial function in patients with ischemic cardiomyopathy.
The adjustment of medications and dosages to the needs of individual patients with heart failure is mostly intuitive, but even when their effect on global myocardial function is measured by classic indexes, their effect on segmental function is overlooked. This study was conducted to assess the feasibility of using echocardiographic myocardial strain imaging to evaluate the effect of medication on global and segmental function in 21 ambulatory patients with heart failure (mean age 65+/-11 years) who had echocardiographic studies performed before and 2 hours after ingesting their regular morning medications. The ejection fraction, global and regional strain, and time to regional peak strain were compared between the 2 examinations. Medication induced no significant changes in mean ejection fraction (28.6+/-7.8% to 27.5+/-9.9%) and mean global strain (-9.5+/-3.6% to -9.8+/-3.2%). Changes in segmental strain depended on baseline function: normal segments (peak strain more negative than -12%) deteriorated (-15.5+/-2.7% to -13.7+/-4.6%, p<0.0001), but dysfunctional segments (peak strain less negative than -8%) improved (-5.3+/-2.0% to -7.4+/-4.3%, p<0.0001). Medication also improved segmental synchronization: average time to peak strain of segments in which peak strain was attained before aortic valve closure increased (325+/-69 to 375+/-100 ms, p<0.0001), but that of segments with postsystolic shortening at baseline decreased (451+/-93 to 435+/-93 ms, p<0.006). Thus, the time interval between time to peak strain of segments with systolic and post-systolic shortening at baseline was halved after medication. In conclusion, medications for heart failure induced an increase in the echocardiographically determined peak strain of myocardial segments with impaired function at baseline but decreased the peak strain of normally contracting segments. Medications also improved the synchronization of myocardial contraction. Neither the global ejection fraction nor global strain reflected these changes. Thus, medication tended to improve the homogeneity of left ventricular contraction.
Blondheim
David S
DS
Unit of Noninvasive Cardiology, Department of Cardiology, Hillel-Yaffe Medical Center, Hadera, Rappaport Faculty of Medicine, Technion, Israel. blond@netvision.net.il
Kazatsker
Mark
M
Friedman
Zvi
Z
Lysyansky
Peter
P
Meisel
Simcha R
SR
Asif
Aya
A
Smirin
Nahum
N
Shotan
Avraham
A
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use*; D000368:Aged; D000369:Aged, 80 and over; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology / Q000627:therapeutic use*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology / Q000627:therapeutic use; D001696:Biomechanical Phenomena; D002311:Cardiomyopathy, Dilated / Q000188:drug therapy*; D004232:Diuretics / Q000494:pharmacology / Q000627:therapeutic use*; D015150:Echocardiography, Doppler; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000187:drug effects*
D000319:Adrenergic beta-Antagonists; D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D000889:Anti-Arrhythmia Agents; D004232:Diuretics