Cardiac magnetic resonance imaging provides new insight into hypertensive heart disease—a reply

To the Editor We thank the readers for their interest in our article.1 With regards to the request for correlation with office and ambulatory blood pressure readings, these data are provided in the manuscript: end-diastolic wall thickness correlated with office systolic blood pressure (R=.43, P<.01) and office diastolic blood pressure (R=.32, P<.005) but did not correlate with ambulatory blood pressure monitoring systolic blood pressure (R=.24, P=.12), ambulatory blood pressure monitoring diastolic blood pressure (R=.18, P=.27), or ambulatory blood pressure monitoring systolic mean arterial pressure (R=.18, P=.27). We agree that echocardiography is currently the imaging modality most frequently used to investigate patients with arterial hypertension, but cardiovascular magnetic resonance imaging has the potential to offer a “one-stop” comprehensive assessment of patients with hypertension, both to screen for secondary causes and identify target organ damage.2 We elected to perform cardiovascular magnetic resonance imaging rather than echocardiography because of its increased tissue contrast and because of its superior ability to image subjects with concomitant obesity consistently. We did not perform a direct comparison of echocardiographic and cardiovascular magnetic resonance imaging findings but agree it would be interesting to perform such a study in the future. We also agree that left ventricular (LV) geometry is an interesting parameter. We provide data on absolute wall thickening relative to the LV end-diastolic diameter to correct for changes in LV cavity size. Absolute wall thickening is determined by both end-diastolic wall thickness and radial strain. The proportional decrease in cavity size during systole is more closely determined by end-diastolic dimension than volume. Correction of one-dimensional measurement (absolute wall thickening) by another one-dimensional measurement (diameter) intuitively makes more sense than by a three-dimensional measurement (volume). We provided information on longitudinal shortening, which is mathematically equivalent to longitudinal engineering strain (but with an opposite sign). We chose to calculate midwall myocardial shortening instead of mean circumferential strain as there is a large strain gradient between the epicardium and endocardium. The interaction between diffuse myocardial interstitial fibrosis and myocardial mechanics in hypertensive heart disease is an interesting area. Further to the study by Kuruvilla and colleagues,3 our group has shown that the prevalence and degree of LV fibrosis and central aortic distensibility vary among different hypertensive heart disease LV phenotypes.4, 5 We agree that such new insights are important in advancing our understanding of the pathophysiology of hypertensive heart disease and our appreciation of different potential etiologies and drivers of the hypertensive state. Such insights should help us tailor existing antihypertensive treatments more effectively and highlight potential substrates for new antihypertensive strategies. Dr Chiara Bucciarelli-Ducci is a consultant for Circle Cardiovascular Imaging Inc., Calgary, Canada.