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Left ventricular asynchrony: an indicator of regional myocardial dysfunction
Insights
Left ventricular asynchrony, measured by postejection thickening (PET) and phase difference (PD), effectively quantifies regional myocardial dysfunction severity during ischemia and reperfusion. This method is reliable even without knowing normal baseline function.
Area of Science:
- Cardiology
- Physiology
Background:
- Assessing regional myocardial dysfunction is challenging due to natural variations in wall thickening.
- Absolute values of systolic wall thickening are unreliable for detecting localized dysfunction.
Purpose of the Study:
- To investigate if left ventricular asynchrony can quantify regional myocardial dysfunction severity during ischemia and reperfusion.
- To determine if asynchrony measures are useful when baseline function is unknown.
Main Methods:
- Used sonomicrometry in dogs to measure regional myocardial wall thickness under control, ischemic, and reperfusion conditions.
- Calculated two indexes of left ventricular asynchrony: postejection thickening (PET) and phase difference (PD).
Main Results:
- Systolic wall thickening decreased significantly with increasing ischemia severity.
- PET and PD increased progressively with ischemia severity.
- Inverse linear relationships were found between systolic wall thickening and both PET and PD (r = -0.86 and -0.87, respectively).
- Inotropic stimulation affected wall thickening but not asynchrony levels.
- PET and PD did not correlate with late reperfusion contractile function recovery.
Conclusions:
- Left ventricular asynchrony (PET and PD) can reliably quantify regional myocardial dysfunction severity, even without known baseline function.
- Asynchrony measures are valuable for assessing myocardial dysfunction during ischemia and reperfusion.
- PET and PD are not predictive markers for the functional recovery of myocardium after reperfusion.
Abstract:
There is a marked heterogeneity of myocardial wall thickening within the left ventricle and among different individuals. It is therefore difficult to detect regional myocardial dysfunction from absolute values of systolic wall thickening. We tested whether the extent of left ventricular asynchrony during ischemia and reperfusion can be used to quantify the severity of regional myocardial dysfunction when nonischemic baseline function is not known. In six anesthetized, open-chest dogs regional myocardial wall thickness was measured by means of sonomicrometry under control conditions, at three degrees of ischemic dysfunction (mild, moderate, and severe), and after release of a 15-minute occlusion of the left circumflex coronary artery, when degrees of moderate and mild reperfusion dysfunction similar to the preceding ischemic dysfunction were present. Two indexes of left ventricular asynchrony were calculated: (1) postejection thickening (PET) and (2) the phase difference of the first Fourier harmonic of posterior versus anterior myocardial wall motion (PD). Systolic myocardial wall thickening was decreased from 15.3 +/- 3.1 (standard deviation) % (control value) to 9.7 +/- 1.4% (mild ischemia), 4.2 +/- 1.6% (moderate ischemia), and -3.7 +/- 3.1% (severe ischemia). Conversely PET increased from 0.02 +/- 0.04 mm (control value) to 0.15 +/- 0.22 mm (mild ischemia), 0.19 +/- 0.15 mm (moderate ischemia), and 0.50 +/- 0.26 mm (severe ischemia). PD increased from 9 +/- 28 degrees (control value) to 22 +/- 19 degrees (mild ischemia), 54 +/- 18 degrees (moderate ischemia), and 107 +/- 21 degrees (severe ischemia). After release of the 15-minute left circumflex coronary artery occlusion, PET and PD recovered to 0.34 +/- 0.19 mm and 36 +/- 24 degrees (moderate dysfunction) and 0.25 +/- 0.31 mm and 29 +/- 8 degrees (mild dysfunction), respectively. There were inverse linear relationships between systolic wall thickening and PET (r = -0.86, p less than 0.001) and between systolic wall thickening and PD (r = -0.87, p less than 0.001). Inotropic stimulation by postextrasystolic potentiation increased regional systolic myocardial posterior and anterior wall thickening but did not alter the extent of left ventricular asynchrony. Thus, when normal baseline function is not known, the severity of regional myocardial dysfunction at a given inotropic state can be determined by analysis of left ventricular asynchrony. There was no significant correlation between the extent of PET and PD during ischemia and at early reperfusion and the recovery of contractile function at late reperfusion. Thus PET does not provide a prospective marker for the functional outcome of reperfusion.