Background Surgical ventricular reconstruction is a specific procedure designed to reduce left ventricular volume in patients with heart failure caused by coronary artery disease. We conducted a trial to address the question of whether surgical ventricular reconstruction added to coronary-artery bypass grafting (CABG) would decrease the rate of death or hospitalization for cardiac causes, as compared with CABG alone. Methods Between September 2002 and January 2006, a total of 1000 patients with an ejection fraction of 35% or less, coronary artery disease that was amenable to CABG, and dominant anterior left ventricular dysfunction that was amenable to surgical ventricular reconstruction were randomly assigned to undergo either CABG alone (499 patients) or CABG with surgical ventricular reconstruction (501 patients). The primary outcome was a composite of death from any cause and hospitalization for cardiac causes. The median follow-up was 48 months. Results Surgical ventricular reconstruction reduced the end-systolic volume index by 19%, as compared with a reduction of 6% with CABG alone. Cardiac symptoms and exercise tolerance improved from baseline to a similar degree in the two study groups. However, no significant difference was observed in the primary outcome, which occurred in 292 patients (59%) who were assigned to undergo CABG alone and in 289 patients (58%) who were assigned to undergo CABG with surgical ventricular reconstruction (hazard ratio for the combined approach, 0.99; 95% confidence interval, 0.84 to 1.17; P = 0.90). Conclusions Adding surgical ventricular reconstruction to CABG reduced the left ventricular volume, as compared with CABG alone. However, this anatomical change was not associated with a greater improvement in symptoms or exercise tolerance or with a reduction in the rate of death or hospitalization for cardiac causes. (ClinicalTrials. gov number, NCT00023595.)

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Coronary Bypass Surgery with or without Surgical Ventricular Reconstruction

In acute myocardial infarction (MI), reactive oxygen species (ROS) are generated in the ischaemic myocardium especially after reperfusion. ROS directly injure the cell membrane and cause cell death. However, ROS also stimulate signal transduction to elaborate inflammatory cytokines, e.g. tumour necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and -6, in the ischaemic region and surrounding myocardium as a host reaction. Inflammatory cytokines also regulate cell survival and cell death in the chain reaction with ROS. Both ROS and inflammatory cytokines are cardiodepressant mainly due to impairment of intracellular Ca(2+) homeostasis. Inflammatory cytokines stimulate apoptosis through a TNF-alpha receptor/caspase pathway, whereas Ca(2+) overload induced by extensive ROS generation causes necrosis through enhanced permeability of the mitochondrial membrane (mitochondrial permeability transition). Apoptosis signal-regulating kinase-1 (ASK1) is an ROS-sensitive, mitogen-activated protein kinase kinase kinase that is activated by many stress signals and can activate nuclear factor kappaB and other transcription factors. ASK1-deficient mice demonstrate that the ROS/ASK1 pathway is involved in necrotic as well as apoptotic cell death, indicating that ASK1 may be a therapeutic target to reduce left ventricular (LV) remodelling after MI. ROS and inflammatory cytokines activate matrix metalloproteinases which degrade extracellular matrix, causing a slippage of myofibrils and hence LV dilatation. Consequently, collagen deposition is increased and tissue repair is enhanced with myocardial fibrosis and angiogenesis. Since the extent of LV remodelling is a major predictor of prognosis of the patients with MI, the therapeutic approach to attenuating LV remodelling is critically important.

/pdf/oxidative-stress-and-left-ventricular-remodelling-after-43g6xjgkpg.pdf

Oxidative stress and left ventricular remodelling after myocardial infarction

Chronic heart failure (HF) affects 5 million patients in the United States and is responsible for &1 million hospitalizations and 300 000 deaths annually.1 The total annual costs associated with this disorder have been estimated to exceed $40 billion.1,2 Chronic HF is the only category of cardiovascular diseases for which the prevalence, incidence, hospitalization rate, total burden of mortality, and costs have increased in the past 25 years.1,2 Fueling this epidemic is the increasing number of elderly patients developing impaired left ventricular (LV) function as a manifestation of chronic coronary artery disease (CAD).1,2 With the aging of the population and decline in mortality of other forms of cardiovascular diseases, it is likely that the incidence of HF and its impact on public health will continue to increase.1–3

In the past 3 decades, considerable attention has focused on LV dysfunction, loading conditions, neuroendocrine activation, and ventricular remodeling as the principal pathophysiological mechanisms underlying HF progression.4 There has been a fundamental shift, however, in the origin of HF that often is underemphasized.3–5 The Framingham Heart Study suggests that the most common cause of HF is no longer hypertension or valvular heart disease, as it was in previous decades, but rather CAD.4

This shift may be related to improved survival of patients after acute myocardial infarction (MI). Over the past 40 years in the United States, the odds of previous MI as a cause for HF increased by 26% per decade in men and 48% per decade in women. In contrast, there has been a 13% decrease per decade for hypertension as a cause of HF in men and a 25% decrease in women, as well as a decrease in valvular disease by 24% per decade in men and 17% in women.

In the 24 …

Navigating the crossroads of coronary artery disease and heart failure.

Published by Elsevier B.V. on behalf of the Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.

National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Guidelines for the Prevention, Detection, and Management of Heart Failure in Australia 2018

Background— Heart failure remains a significant problem. Tissue-engineered cardiac patches offer potential to treat severe heart failure. We studied an extracellular matrix scaffold for repairing the infarcted left ventricle.

Methods and Results— Pigs (n=42) underwent left ventricular (LV) infarction. At 6 to 8 weeks, either 4-layer multilaminate urinary bladder-derived extracellular matrix or expanded polytetrafluoroethlyene (ePTFE) was implanted as full-thickness LV wall patch replacement. At 1-week, 1-month, or 3-month intervals, pigs were terminated. After macroscopic examination, samples of tissue were prepared for histology, immunocytochemistry, and analysis of cell proportions by flow cytometry. One-week and 1-month patches were intact with thrombus and inflammation; at 1 month, there was also tissue with spindle-shaped cells in proteoglycan-rich and collagenous matrix. More α-smooth muscle actin-positive cells were present in urinary bladder matrix (UBM) than in ePTFE (22.2±3.3% versus 8.4±2.7%; P =0.04). At 3 months, UBM was bioresorbed, and a collagen-rich vascularized tissue with numerous myofibroblasts was present. Isolated regions of α-sarcomeric actin-positive, intensely α-smooth muscle actin-immunopositive, and striated cells were observed. ePTFE at 3 months had foreign-body response with necrosis and calcification. Flow cytometry showed similarities of cells from UBM to normal myocardium, whereas ePTFE had limited cardiomyocyte markers.

Conclusions— Appearance of a fibrocellular tissue that included contractile cells accompanied biodegradation of UBM when implanted as an LV-free wall infarction patch. UBM appears superior to synthetic material for cardiac patching and trends toward myocardial replacement at 3 months.

Extracellular Matrix Scaffold for Cardiac Repair

Surgical ventricular restoration in the treatment of congestive heart failure due to post-infarction ventricular dilation.

https://www.annalsthoracicsurgery.org/article/S0003-4975(06)00660-6/pdf

Left Ventricular Wall Stress in Patients With Severe Aortic Insufficiency With Finite Element Analysis

https://www.internationaljournalofcardiology.com/article/S0167-5273(15)30725-7/pdf

Successful use of 20 mm SAPIEN 3 for valve-in-valve intervention within a 19 mm degenerated aortic bioprosthetic valve

From academics to practice.

J Thorac Cardiovasc Surg 1999;117:111-116 Barzilai Victor G. Davila-Roman, Nicholas T. Kouchoukos, Kenneth B. Schechtman and BenicoRENAL DYSFUNCTION AFTER CARDIAC OPERATIONS ATHEROSCLEROSIS OF THE ASCENDING AORTA IS A PREDICTOR OFhttp://jtcs.ctsnetjournals.org/cgi/content/full/117/1/111 the World Wide Web at: The online version of this article, along with updated information and services, is located on

Nicholas T. Kouchoukos

Papers

Surgical ventricular restoration in the treatment of congestive heart failure due to post-infarction ventricular dilation.

Left Ventricular Wall Stress in Patients With Severe Aortic Insufficiency With Finite Element Analysis

Successful use of 20 mm SAPIEN 3 for valve-in-valve intervention within a 19 mm degenerated aortic bioprosthetic valve

From academics to practice.

Renal dysfunction after cardiac operations atherosclerosis of the ascending aorta is a predictor of