J. Michael DiMaio M.D.

Fann, J. I., S. D. Moffatt-Bruce, J. M. DiMaio and J. A. Sanchez (2016). “Human factors and human nature in cardiothoracic surgery.” Ann Thorac Surg Apr 27 [Epub ahead of print].

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Surgical errors and adverse events include wrong or delayed operations and judgment lapses that lead to incorrect procedures 3, 4, 5, 6 and 7. It is estimated that 54% of the adverse events in patients undergoing operations surgery are preventable [7]. In patients undergoing coronary artery bypass grafting, for whom the risk-adjusted mortality rate ranges from 1.3% to 3.1%, approximately one-third of associated deaths may be preventable, with most occurring in the operating room and intensive care unit [6]. Surgical outcomes are often attributed primarily to the technical skills of the surgeon: when errors are made, the surgeon’s competence is questioned 3, 4, 8, 9 and 10. The notion that the surgeon is often held solely accountable is evidenced in the basis for surgeon rankings in public reporting.

Hebeler, K. R., J. J. Squiers, M. Arsalan, H. Baumgarten, D. O. Moore, W. H. Ryan, M. J. Mack, P. Grayburn and J. M. DiMaio (2016). “Aortic regurgitation caused by an aberrant mitral chord tethering the anterior mitral leaflet to an aortic valve cusp.” Ann Thorac Surg 101(5): e163.

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A 37-year-old man, active military, with a known heart murmur presented with new onset dyspnea on significant exertion. Transesophageal echocardiography revealed a subaortic fibrous strand connecting the A2 portion of the mitral valve to the left coronary cusp of the aortic valve, resulting in cusp prolapse and eccentric severe aortic regurgitation (Fig 1, Video). To facilitate surgical excision, transverse aortotomy was performed through an upper partial sternotomy. The abnormal chorda was resected from the underside of the aortic leaflet to the free edge of the mitral leaflet (Fig 2). After the resection, residual prolapse of the left coronary cusp was visualized, so a commissuroplasty was performed to shore up the redundant edges of the leaflet. After aortic closure, two areas of trace-to-mild aortic insufficiency, normal aortic leaflet opening motion, and trace mitral regurgitation were observed by transesophageal echocardiography. The chord was 2.5 cm long and composed of tan-white soft tissue (Fig 3) without necrosis, myxoid degeneration, calcification, or inflammation.

Baumgarten, H., J. J. Squiers, M. Arsalan, J. M. Dimaio and M. J. Mack (2016). “Defining the clinical need and indications: who are the right patients for transcatheter mitral valve replacement?” J Cardiovasc Surg (Torino). Mar 30. [Epub ahead of print]

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Mitral regurgitation (MR) can be divided into two major etiologies, primary and secondary MR. Primary MR, also termed degenerative or organic MR, is a disease of the valve itself and is treated routinely by surgical repair in all but prohibitive risk patients. In these patients, transcatheter repair techniques, including edge to edge repair with the MitraClip device have been largely successful and widely adopted. Transcatheter placement of artificial chords has also been performed. The potential role for transcatheter mitral valve replacement (TMVR) in primary MR will likely be quite limited. Secondary or functional MR is due to a disease of the left ventricle and not the valve itself. The MR is a result of dilation of the left ventricle causing distraction of the papillary muscles with tethering of the mitral leaflets and lack of leaflet coaptation. Medical therapy is the mainstay treatment, with resynchronization used in appropriate patients. Surgical repair, usually with an undersized annuloplasty, is used in a limited number of patients. Transcatheter edge to edge repair is used extensively outside the US in secondary MR and is the subject of a pivotal trial in the US. However, it is in this group of patients with secondary MR that there is the largest clinical unmet need and, hence, the greatest potential opportunity for transcatheter mitral valve replacement (TMVR). At least ten TMVR platforms are in early feasibility, first in human, or preclinical trial stages. Four devices have cumulative early human experience in <100 patients. In this article, we discuss those patients most likely to benefit from TMVR and detail lessons learned from the first human studies regarding patient selection.

Thatcher, J. E., W. Li, Y. Rodriguez-Vaqueiro, J. J. Squiers, W. Mo, Y. Lu, K. D. Plant, E. Sellke, D. R. King, W. Fan, J. A. Martinez-Lorenzo and J. M. DiMaio (2016). “Multispectral and Photoplethysmography Optical Imaging Techniques Identify Important Tissue Characteristics in an Animal Model of Tangential Burn Excision.” J Burn Care Res 37(1): 38-52.

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Burn excision, a difficult technique owing to the training required to identify the extent and depth of injury, will benefit from a tool that can cue the surgeon as to where and how much to resect. We explored two rapid and noninvasive optical imaging techniques in their ability to identify burn tissue from the viable wound bed using an animal model of tangential burn excision. Photoplethysmography (PPG) imaging and multispectral imaging (MSI) were used to image the initial, intermediate, and final stages of burn excision of a deep partial-thickness burn. PPG imaging maps blood flow in the skin’s microcirculation, and MSI collects the tissue reflectance spectrum in visible and infrared wavelengths of light to classify tissue based on a reference library. A porcine deep partial-thickness burn model was generated and serial tangential excision accomplished with an electric dermatome set to 1.0 mm depth. Excised eschar was stained with hematoxylin and eosin to determine the extent of burn remaining at each excision depth. We confirmed that the PPG imaging device showed significantly less blood flow where burn tissue was present, and the MSI method could delineate burn tissue in the wound bed from the viable wound bed. These results were confirmed independently by a histological analysis. We found these devices can identify the proper depth of excision, and their images could cue a surgeon as to the preparedness of the wound bed for grafting. These image outputs are expected to facilitate clinical judgment in the operating room.

Squiers, J. J., K. B. Harrington, M. Arsalan and J. M. DiMaio (2016). “Preventative medicine: The next revolution in the treatment of aortic stenosis.” Journal of Thoracic and Cardiovascular Surgery 151(1): 263-264.

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Calcific aortic stenosis (AS) has been the most common indication for surgical valve replacement in the developed world for decades. The pathophysiology of aortic valve (AV) calcification is driven by 3 interrelated mechanisms: (1) classical cardiovascular risk factors, (2) genetic factors, and (3) valve cellular biology. Although AV calcification was long believed to be a passive process (“degenerative” valve disease), a growing body of literature has demonstrated that the progression of calcification on the AV is actively regulated. The natural progression of calcific AV disease was first described by Otto and colleagues. The initial stage of AV calcification, called valve sclerosis, is associated with focal leaflet thickening that leads to calcification without hemodynamic consequences. Eventually leaflet thickening and calcification obstruct the left ventricular outflow tract, causing hemodynamic changes and a resulting diagnosis of AS. Notably, aortic sclerosis is slow to progress to AS, which is the primary reason AS is typically considered a disease of the elderly. AS ultimately leads to heart failure, and the major predictor of mortality for this pathology is the onset of associated symptoms, left ventricular dysfunction, or both. Despite the rapid growth in our understanding of the etiology of AV calcification, no preventive strategy for AS is currently available. Currently, there are an estimated 500,000 elderly people (age ≥75 years) with severe symptomatic AS living in the United States, a number that is expected to triple by 2050.