Gergely Szantho

Remote ischaemic postconditioning protects the heart during acute myocardial infarction in pigs

Background: Ischaemic preconditioning results in a reduction in ischaemic-reperfusion injury to the heart. This beneficial effect is seen both with direct local preconditioning of the myocardium and with remote preconditioning of easily accessible distant non-vital limb tissue. Ischaemic postconditioning with a comparable sequence of brief periods of local ischaemia, when applied immediately after the ischaemic insult, confers benefits similar to preconditioning. Objective: To test the hypothesis that limb ischaemia induces remote postconditioning and hence reduces experimental myocardial infarct size in a validated swine model of acute myocardial infarction. Methods: Acute myocardial infarction was induced in 24 pigs with 90 min balloon inflations of the left anterior descending coronary artery. Remote ischaemic postconditioning was induced in 12 of the pigs by four 5 min cycles of blood pressure cuff inflation applied to the lower limb immediately after the balloon deflation. Infarct size was assessed by measuring 72 h creatinine kinase release, MRI scan and immunohistochemical analysis. Results: Area under the curve of creatinine kinase release was significantly reduced in the postconditioning group compared with the control group with a 26% reduction in the infarct size (p<0.05). This was confirmed by MRI scanning and immunohistochemical analysis that revealed a 22% (p<0.05) and a 47.52% (p<0.01) relative reduction in the infarct size, respectively. Conclusion: Remote ischaemic postconditioning is a simple technique to reduce infarct size without the hazards and logistics of multiple coronary artery balloon inflations. This type of conditioning promises clear clinical potential.

The Relationship Between Left Ventricular Wall Thickness, Myocardial Shortening, and Ejection Fraction in Hypertensive Heart Disease: Insights From Cardiac Magnetic Resonance Imaging

Hypertensive heart disease is often associated with a preserved left ventricular ejection fraction despite impaired myocardial shortening. The authors investigated this paradox in 55 hypertensive patients (52±13 years, 58% male) and 32 age‐ and sex‐matched normotensive control patients (49±11 years, 56% male) who underwent cardiac magnetic resonance imaging at 1.5T. Long‐axis shortening (R=0.62), midwall fractional shortening (R=0.68), and radial strain (R=0.48) all decreased (P<.001) as end‐diastolic wall thickness increased. However, absolute wall thickening (defined as end‐systolic minus end‐diastolic wall thickness) was maintained, despite the reduced myocardial shortening. Absolute wall thickening correlated with ejection fraction (R=0.70, P<.0001). In multiple linear regression analysis, increasing wall thickness by 1 mm independently increased ejection fraction by 3.43 percentage points (adjusted β‐coefficient: 3.43 [2.60–4.26], P<.0001). Increasing end‐diastolic wall thickness augments ejection fraction through preservation of absolute wall thickening. Left ventricular ejection fraction should not be used in patients with hypertensive heart disease without correction for degree of hypertrophy.

Use of Radiofrequency Perforation for Lead Placement in Biventricular or Conventional Endocardial Pacing after Mustard or Senning Operations for D‐Transposition of the Great Arteries

Background: Endocardial pacemaker lead placement can be challenging after Mustard and Senning operations for transposition of the great arteries (D‐TGA), if there is atresia of the systemic venous pathways and because the coronary sinus cannot be used for cardiac resynchronization therapy. Radiofrequency (RF)‐assisted perforation techniques have been used in congenital heart disease but have not been reported for use in pacemaker implantation.

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: enddiastolic 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 “onestop” 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 enddiastolic diameter to correct for changes in LV cavity size. Absolute wall thickening is determined by both enddiastolic wall thickness and radial strain. The proportional decrease in cavity size during systole is more closely determined by enddiastolic dimension than volume. Correction of onedimensional measurement (absolute wall thickening) by another onedimensional measurement (diameter) intuitively makes more sense than by a threedimensional 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.

The relationship between left ventricular wall thickness, myocardial shortening and ejection fraction in hypertensive heart disease

Hypertensive heart disease is often associated with a preserved left ventricular ejection fraction despite impaired myocardial shortening. The authors investigated this paradox in 55 hypertensive patients (52±13 years, 58% male) and 32 age‐ and sex‐matched normotensive control patients (49±11 years, 56% male) who underwent cardiac magnetic resonance imaging at 1.5T. Long‐axis shortening (R=0.62), midwall fractional shortening (R=0.68), and radial strain (R=0.48) all decreased (P<.001) as end‐diastolic wall thickness increased. However, absolute wall thickening (defined as end‐systolic minus end‐diastolic wall thickness) was maintained, despite the reduced myocardial shortening. Absolute wall thickening correlated with ejection fraction (R=0.70, P<.0001). In multiple linear regression analysis, increasing wall thickness by 1 mm independently increased ejection fraction by 3.43 percentage points (adjusted β‐coefficient: 3.43 [2.60–4.26], P<.0001). Increasing end‐diastolic wall thickness augments ejection fraction through preservation of absolute wall thickening. Left ventricular ejection fraction should not be used in patients with hypertensive heart disease without correction for degree of hypertrophy.

The relationship between left ventricular wall thickness, myocardial shortening and ejection fraction in hypertensive heart disease: insights from cardiac magnetic resonance: LVH independently augments EF in hypertension

Hypertensive heart disease is often associated with a preserved left ventricular ejection fraction despite impaired myocardial shortening. The authors investigated this paradox in 55 hypertensive patients (52±13 years, 58% male) and 32 age‐ and sex‐matched normotensive control patients (49±11 years, 56% male) who underwent cardiac magnetic resonance imaging at 1.5T. Long‐axis shortening (R=0.62), midwall fractional shortening (R=0.68), and radial strain (R=0.48) all decreased (P<.001) as end‐diastolic wall thickness increased. However, absolute wall thickening (defined as end‐systolic minus end‐diastolic wall thickness) was maintained, despite the reduced myocardial shortening. Absolute wall thickening correlated with ejection fraction (R=0.70, P<.0001). In multiple linear regression analysis, increasing wall thickness by 1 mm independently increased ejection fraction by 3.43 percentage points (adjusted β‐coefficient: 3.43 [2.60–4.26], P<.0001). Increasing end‐diastolic wall thickness augments ejection fraction through preservation of absolute wall thickening. Left ventricular ejection fraction should not be used in patients with hypertensive heart disease without correction for degree of hypertrophy.

Comprehensive intra/extracellular myocardial structural and functional characterization of hypertensive heart disease phenotypes

Background The European Society of Cardiology recognizes different hypertensive heart disease (HHD) phenotypes. HHD can be classified into 4 left ventricular (LV) phenotypes by indexed LV mass, mass to volume ratio (M:V) and indexed end diastolic volume (EDV) (Table 1). All remodeling/ hypertrophy phenotypes carry adverse cardiovascular prognosis, but the underlying mechanisms are incompletely understood. We investigated differences in intra/extracellular myocardial structure and function between phenotypes with T1 mapping and myocardial strain analysis.

Cardiac pre-load alteration with MRI-compatible lower body suction device.

Background Our group studies circulatory causes of exercise limitation in congenital heart patients with dilated right ventricle, but normal resting left ventricular ejection fraction. Cardiac MRI is the gold standard non-invasive tool for measuring heart chamber volume and blood vessel flow. We designed an MRI-compatible lower body negative pressure (LBNP) device (Image) in order to study the effect of pre-load reduction on the heart with MRI. This is a pilot study to establish our methodology.

Validation of segmented and real-time EPI phase contrast flow quantification against segmented gradient echo sequences

Background MR based Flow Quantification is an established method for measuring cardio-pulmonary haemodynamics, but is challenging to perform in situations where it may be advantageous to asses real-world physiological behavior, for example in exercise. The availability of a new real time flow quantification sequence presents the opportunity to measure velocity and flow without these challenges. This study is a preliminary validation of the method as a precursor to use of the sequence in subjects undergoing assessment of induced haemodynamic change by exercise and preload alteration. Methods

Measuring ventricular volumes during exercise with vertical long axis cines

Background Imaging cardiac function during exercise remains difficult. Some researchers interrupted the exercise to obtain data, but this is not physiological. Others used real time short axis cine imaging, which presents issues with respiratory motion. La Gerche et al (Circ. Cardiovasc. Imaging 2013) may have solved this by linking the short axis images to the respiratory cycle with additional long axis imaging, but using a not widely available in-house software. We set out to explore a feasible alternative method of scanning and analysis.