The non-invasive quantification of regional myocardial function is an important goal in clinical cardiology. Myocardial thickening/thinning indices is one method of attempting to define regional myocardial function. A new ultrasonic method of quantifying regional deformation has been introduced based on the principles of 'strain' and 'strain rate' imaging. These new imaging modes introduce concepts derived from mechanical engineering which most echocardiographers are not familiar with. In order to maximally exploit these new techniques, an understanding of what they measure is indispensable. This paper will define each of these modalities in terms of physical principles and will give an introduction to the principles of data acquisition and processing required to implement ultrasonic strain and strain rate imaging. In addition, the current status of development of the technique and its limitations will be discussed, together with examples of potential clinical applications.

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BACKGROUND The role of assessment of myocardial viability in identifying patients with ischemic cardiomyopathy who might benefit from surgical revascularization remains controversial. Furthermore, although improvement in left ventricular function is one of the goals of revascularization, its relationship to subsequent outcomes is unclear. METHODS Among 601 patients who had coronary artery disease that was amenable to coronaryartery bypass grafting (CABG) and who had a left ventricular ejection fraction of 35% or lower, we prospectively assessed myocardial viability using single-photonemission computed tomography, dobutamine echocardiography, or both. Patients were randomly assigned to undergo CABG and receive medical therapy or to receive medical therapy alone. Left ventricular ejection fraction was measured at baseline and after 4 months of follow-up in 318 patients. The primary end point was death from any cause. The median duration of follow-up was 10.4 years. RESULTS CABG plus medical therapy was associated with a lower incidence of death from any cause than medical therapy alone (182 deaths among 298 patients in the CABG group vs. 209 deaths among 303 patients in the medical-therapy group; adjusted hazard ratio, 0.73; 95% confidence interval, 0.60 to 0.90). However, no significant interaction was observed between the presence or absence of myocardial viability and the beneficial effect of CABG plus medical therapy over medical therapy alone (P = 0.34 for interaction). An increase in left ventricular ejection fraction was observed only among patients with myocardial viability, irrespective of treatment assignment. There was no association between changes in left ventricular ejection fraction and subsequent death. CONCLUSIONS The findings of this study do not support the concept that myocardial viability is associated with a long-term benefit of CABG in patients with ischemic cardiomyopathy. The presence of viable myocardium was associated with improvement in left ventricular systolic function, irrespective of treatment, but such improvement was not related to long-term survival. (Funded by the National Institutes of Health; STICH ClinicalTrials.gov number, .)

A specific LV mechanical dyssynchrony pattern, characterized by ApRock and SF, is associated with a more favourable long-term survival after CRT. Both parameters are also indicators of an effective therapy.

Background Left ventricular non-compaction (LVNC) is a genetically and phenotypically heterogeneous disease and, although increasingly recognized in clinical practice, there is a lack of widely accepted diagnostic criteria. We sought to identify novel genetic causes of LVNC and describe genotype-phenotype correlations. Methods and Results 190 patients from 174 families with left ventricular hypertrabeculation (LVHT) or LVNC were referred for cardiac magnetic resonance and whole exome sequencing. 425 control individuals were included to identify variants of interest (VOIs). We found an excess of 138 VOIs in 102 (59%) unrelated patients in 54 previously identified LVNC or other known cardiomyopathy genes. VOIs were found in 68 of 90 probands with LVNC and 34 of 84 probands with LVHT (76% and 40%, respectively; p<0.001). We identified 0, 1, and ≥2 VOIs in 72, 74, and 28 probands, respectively. We found increasing number of VOIs in a patient strongly correlated with several markers of disease severity, including ratio of non-compacted to compacted myocardium (p<0.001) and left ventricular ejection fraction (p=0.01). The presence of sarcomeric gene mutations was associated with increased occurrence of late gadolinium enhancement (p=0.004). Conclusions LVHT and LVNC likely represent a continuum of genotypic disease with differences in severity and variable phenotype explained, in part, by the number of VOIs and whether mutations are present in sarcomeric or non-sarcomeric genes. Presence of VOIs is common in patients with LVHT. Our findings expand the current clinical and genetic diagnostic approaches for patients with LVHT and LVNC.

Background-We sought to investigate ultrasonic strain rate and strain as new indices to quantify the contractile reserve of stunned myocardium during dobutamine infusion. Methods and Results-Stunning of the left ventricular posterior wall was induced in 9 closed-chest pigs after 30 minutes of severe hypoperfusion followed by 60 minutes of reperfusion of the left circumflex coronary artery territory. A second group of 7 animals had no coronary occlusion and served as normal controls. An incremental dobutamine infusion protocol was used in both groups. Changes in regional radial function were monitored by use of ultrasound-derived maximal systolic radial strain rate (SR) and systolic strain (⑀). In the control group, dobutamine induced an increase in both SR and maximal dP/dt, which correlated linearly (rϭ0.85). Conversely, ⑀ values increased at low doses of dobutamine (2.5 to 5 g · kg Ϫ1 · min

In this model of acute ischemia, ultrasonic strain indexes differentiate acutely ischemic segments from both normal and dysfunctional myocardium. This should be a promising new approach to the bedside monitoring of acute ischemic changes in regional myocardial function.