Marcin Malinowski

Heterogeneity of Left Ventricular Wall Thickening Mechanisms

Background— Myocardial fibers are grouped into lamina (or sheets) 3 to 4 cells thick. Fiber shortening produces systolic left ventricular (LV) wall thickening primarily by laminar extension, thickening, and shear, but the regional variability and transmural distribution of these 3 mechanisms are incompletely understood. Methods and Results— Nine sheep had transmural radiopaque markers inserted into the anterior basal and lateral equatorial LV. Four-dimensional marker dynamics were studied with biplane videofluoroscopy to measure circumferential, longitudinal, and radial systolic strains in the epicardium, midwall, and endocardium. Fiber and sheet angles from quantitative histology allowed transformation of these strains into transmural contributions of sheet extension, thickening, and shear to systolic wall thickening. At all depths, systolic wall thickening in the anterior basal region was 1.6 to 1.9 times that in the lateral equatorial region. Interestingly, however, systolic fiber shortening was identical at each transmural depth in these regions. Endocardial anterior basal sheet thickening was >2 times greater than in the lateral equatorial region (epicardium, 0.16±0.15 versus 0.03±0.06; endocardium, 0.45±0.40 versus 0.17±0.09). Midwall sheet extension was >2 times that in the lateral wall (0.22±0.12 versus 0.09±0.06). Epicardial and midwall sheet shears in the anterior wall were ≈2 times higher than in the lateral wall (epicardium, 0.14±0.07 versus 0.05±0.03; midwall, 0.21±0.12 versus 0.12±0.06). Conclusions— These data demonstrate fundamentally different regional contributions of laminar mechanisms for amplifying fiber shortening to systolic wall thickening. Systolic fiber shortening was identical at each transmural depth in both the anterior and lateral LV sites. However, systolic wall thickening of the anterior site was much greater than that of the lateral site. Fiber shortening drives systolic wall thickening, but sheet dynamics and orientations are of great importance to systolic wall thickening. LV wall thickening and its clinical implications pivot on different wall thickening mechanisms in various LV regions. Attempts to implant healthy contractile cells into diseased hearts or to surgically manipulate LV geometry need to take into account not only cardiomyocyte contraction but also transmural LV intercellular architecture and geometry.

Passive ventricular constraint prevents transmural shear strain progression in left ventricle remodeling

Background— Passive ventricular constraint provides external cardiac support to reduce left ventricular (LV) wall stress and myocardial stretch, which are primary determinants of LV remodeling. Altered wall strain results in cytokine and reactive oxygen species production, which, in turn, stimulates apoptosis and extracellular matrix disruption and could be an important trigger for adverse global LV dilatation and remodeling. The effects of the Acorn cardiac support device (CSD) on regional transmural LV wall strains, however, remain unknown. Methods and Results— Thirty-three sheep had transmural radiopaque beadsets surgically inserted into the anterior basal and lateral equatorial LV walls, with additional markers silhouetting the left ventricle. Eight animals had CSD implanted (myocardial infarction [MI]+CSD). One week thereafter, the MI+CSD group and 10 animals without CSD (MI) underwent posterior LV infarction by snaring obtuse marginal coronary arteries. Fifteen animals (Sham) had no infarction or CSD. 4D marker dynamics were measured with biplane videofluoroscopy 1 and 8 weeks postoperatively. LV volumes, sphericity index, and transmural circumferential, longitudinal, and radial systolic strains were analyzed. Compared with Sham, infarction (MI) dilated the heart, reduced sphericity index (LV length/width), and increased longitudinal–radial shear strains in the inner half of both the anterior and lateral LV walls. CSD prevented this shear strain perturbation, minimized LV end diastolic volume increase, and augmented the LV sphericity index. Conclusions— Prophylactic CSD prevented infarct-induced shear strain progression not only in myocardium adjacent to, but also remote from, the infarct. CSD also prevented LV dilatation and sphericalization. By attenuating shear strain abnormalities, CSD could prevent the heart from entering into a positive feedback loop of further LV dilatation and exaggeration of LV wall stress and may reduce biochemical triggers portending adverse LV remodeling.

Effects of Undersized Mitral Annuloplasty on Regional Transmural Left Ventricular Wall Strains and Wall Thickening Mechanisms

Background— Undersized mitral annuloplasty, widely used for ischemic and functional mitral regurgitation (MR), has been proposed as an “annular solution to a ventricular problem.” Beyond relief of MR, it is thought to improve global left ventricular (LV) shape, hence potentially reducing myocardial stress and promoting beneficial reverse LV remodeling. We previously observed that undersized annuloplasty inhibited systolic wall thickening at the LV base near the mitral annulus. In this study, we measured the effects of undersized annuloplasty on regional transmural LV wall fiber and sheet strains and wall thickening mechanisms. Methods and Results— Nine sheep had transmural radiopaque beadsets surgically inserted into anterobasal and lateral equatorial LV regions, with additional markers silhouetting the LV and mitral annulus. 4-Dimensional marker dynamics were studied with biplane videofluoroscopy before and after tightening an adjustable Paneth-type mitral annuloplasty suture. Transmural circumferential, longitudinal, and radial systolic and remodeling strains in the subepicardium (20% depth), midwall (50%), and subendocardium (80%) in both regions were computed. Fiber and sheet angles from quantitative regional histology allowed transformation of these strains into local fiber (f), sheet (s), and sheet-normal (n) coordinates. Further analysis calculated the transmural contributions of sheet extension (Essc), sheet thickening (Ennc), and sheet shear (Esnc) to systolic wall thickening (E33). In the anterobasal region, undersized annuloplasty reduced systolic wall thickening (E33) by ≈50% at all transmural depths by inhibiting: (1) subendocardial systolic fiber shortening (−0.10±0.05 versus −0.04±0.05; P<0.05); (2) subepicardial (0.16±0.15 versus 0.09±0.08; P<0.05) and subendocardial (0.45±0.40 versus 0.19±0.18; P<0.05) systolic sheet thickening; (3) midwall sheet extension (0.22±0.12 versus 0.11±0.06; P<0.05); and (4) transmural sheet shear (subepicardium, −0.14±0.07 versus −0.08±0.07; midwall, 0.21±0.12 versus 0.10±0.11; subendocardium, −0.19±0.23 versus −0.11±0.16; P<0.05). In the remote lateral equatorial region, fiber-sheet strains and E33 were unchanged. Conclusions— In this acute animal study, undersized annuloplasty inhibited systolic wall thickening in the anterobasal region by reducing subendocardial systolic fiber shortening and laminar sheet wall thickening, but had no effects in a more distant LV region. This suggests that undersized mitral annuloplasty may have potentially deleterious effects on local myocardial mechanics.

The co-application of hypoxic preconditioning and postconditioning abolishes their own protective effect on systolic function in human myocardium.

BACKGROUND Ischemic preconditioning (IPC) and postconditioning (POC) are well documented to trigger cardioprotection against ischemia/reperfusion (I/R) injury, but the effect oftheir both co-application remains unclear in human heart. The present study sought to assessthe co-application of IPC and POC on fragments of human myocardium in vitro. METHODS Muscular trabeculae of the human right atrial were electrically driven in the organbath and subjected to simulated I/R injury - hypoxia/re-oxygenation injury in vitro. To achieveIPC of trabeculae the single brief hypoxia period preceded the applied lethal hypoxia, and to achieve POC triple brief hypoxia periods followed the lethal hypoxia. Additional muscular trabeculae were exposed only to the hypoxic stimulation (Control) or were subjected to the non-hypoxic stimulation (Sham). 10 μM norepinephrine (NE) application ended every experiment to assess viability of trabeculae. The contraction force of the myocardium assessed as a maximal amplitude of systolic peak (%Amax) was obtained during the whole experiments period. RESULTS Co-application of IPC and POC resulted in decrease in %Amax during the re-oxygentaionperiod and after NE application, as compared to Control (30.35 ± 2.25 vs. 41.89 ± 2.25, 56.26 ± 7.73 vs. 65.98 ± 5.39, respectively). This was in contrary to the effects observed when IPC and POC were applied separately. CONCLUSIONS The co-application of IPC and POC abolishes the cardioprotection of either intervention alone against simulated I/R injury in fragments of the human right heart atria.

Coronary artery spasm following on-pump coronary artery bypass grafting with 20 months follow-up

We report on a 69-year-old woman who demonstrated native coronary artery and grafted vessel spasm following on-pump coronary artery bypass grafting (CABG). Despite intraaortic balloon pump (IABP) insertion, electrocardiogram (ECG) abnormalities did not disappear. Emergency coronary angiography (CAG) was performed. The patient was successfully treated with systemic and intracoronary injection of vasodilator agents. ECG changes disappeared, with normalized and stable hemodynamic function. Intraaortic balloon pump was maintained for 48 h. The patient was discharged in good clinical condition. Coronary artery spasm (CAS) may result in life-threatening arrhythmias, circulatory collapse or death. The etiology of CAS is multifactorial and includes heart manipulation, exogenous vasoconstrictors, stress-related catecholamine release, hypoxia and oxidative stress. Postoperative CAS is most commonly manifested by ST-segment elevation and circulatory collapse without specific causes. The gold standard for revealing CAS is CAG. Infusion of vasodilators combined with IABP is adequate in most instances, but extracorporeal membrane oxygenation has been necessary for more extensive or resistant coronary spasm.

A large pseudoaneurysm of the left cardiac ventricle in a 57-year-old patient after urgent coronary artery bypass grafting and surgical mitral valve replacement due to acute myocardial infarction

We present a rare case of a left ventricular pseudoaneurysm in a patient after inferior wall myocardial infarction. The infarction was complicated with acute mitral insufficiency, pulmonary edema, and cardiogenic shock. Urgent surgical mitral valve replacement and coronary artery bypass grafting were performed. After several months, the patient was hospitalized again because of deterioration of exercise tolerance and symptoms of acute congestive heart failure. A large pseudoaneurysm of the left ventricle was recognized and successfully treated surgically.

Different techniques for aortic valve repair and the associated root reconstruction - prospective long-term follow-up of the first 100 patients.

Introduction The advantages of aortic valve and aortic root reconstructive surgery include the provision of natural postoperative valve hemodynamics and the avoidance of prosthetic valve-related complications. A systematic approach based on functional classification of aortic regurgitation allows standardization and reproducibility. Its potential applicability, however, is limited by the relative lack of long-term follow-up data. Aim To achieve the long term results of aortic valve and root repair in prospectively recruited group of 100 patients operated on during first seven years. Material and methods Between the years 2003 and 2013, 225 consecutive patients (175 male, 50 female, mean age 51.3 years) with severe aortic regurgitation and aortic root enlargement underwent aortic valve repair or sparing surgery. The first 100 patients operated between 2003 and 2009 were prospectively enrolled in the study in order to achieve a 105-month follow-up. They underwent aortic valve repair and associated aortic root reconstruction. This prospective study is aimed at assessing the major endpoints of overall survival and freedom from reoperation. Additionally, log-rank testing for the risk factors associated with overall mortality, reoperation, and aortic valve repair failure was performed. Results Among 225 patients, early mortality occurred in the case of 5 patients (2.2%), while 6 (2.5%) patients experienced early valve failure. In a prospective analysis performed on the first 100 patients, long-term results achieved with Kaplan-Meier analysis showed a survival rate of 93% and freedom from reoperation at the level of 91.3%. The risk factors for overall mortality included NYHA class, creatinine level, and perioperative root replacement as reimplantation. Redo operation was associated with bicuspid aortic valve and perioperative leaflet resection with pericardial patch repair. Conclusions One hundred and five month follow-up data from this prospectively analyzed cohort of patients prove that aortic valve repair associated with aortic root reconstruction can be performed with satisfactory results.