A rrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is an inherited disease characterized by a progressive fibrofatty replacement mainly involving the RV myocardium. It is associated with ventricular arrhythmias, heart failure, and sudden cardiac death (SCD).
1-6Clinical Perspective on p 239 RV dilation, reduced RV systolic function, and diffuse RV involvement have previously been studied as predictors of an adverse outcome in patients with ARVC/D but have yielded conflicting results possibly because of divergent imaging modalities, varying parameters measured, and heterogeneous patient cohorts. [7][8][9][10][11][12][13][14][15] Data about the predictive role of RV fractional area change (FAC) in ARVC/D as measured by 2-dimensional transthoracic echocardiography (2D TTE) are scarce and controversial. 9,[14][15][16][17][18][19][20] Tricuspid annulus plane systolic excursion (TAPSE) can easily be determined by M-mode TTE. It is a robust parameter for
Despite the progress made in the prevention and treatment of rejection of the transplanted heart, cardiac allograft vasculopathy (CAV) remains the main cause of death in late survival transplanted patients. CAV consists of a progressive diffuse intimal hyperplasia and the proliferation of vascular smooth muscle cells, ending in wall thickening of epicardial vessels, intramyocardial arteries (50-20 μm), arterioles (20-10 μm), and capillaries (< 10 μm). The etiology of CAV remains unclear; both immunologic and non-immunologic mechanisms contribute to endothelial damage with a sustained inflammatory response. The immunological factors involved are Human Leukocyte Antigen compatibility between donor and recipient, alloreactive T cells and the humoral immune system. The non-immunological factors are older donor age, ischemia-reperfusion time, hyperlipidemia and CMV infections. Diagnostic techniques that are able to assess microvascular function are lacking. Intravascular ultrasound and fractional flow reserve, when performed during coronary angiography, are able to detect epicardial coronary artery disease but are not sensitive enough to assess microvascular changes. Some authors have proposed an index of microcirculatory resistance during maximal hyperemia, which is calculated by dividing pressure by flow (distal pressure multiplied by the hyperemic mean transit time). Non-invasive methods to assess coronary physiology are stress echocardiography, coronary flow reserve by transthoracic Doppler echocardiography, single photon emission computed tomography, and perfusion cardiac magnetic resonance. In this review, we intend to analyze the mechanisms, consequences and therapeutic implications of microvascular dysfunction, including an extended citation of relevant literature data.
Coronary microvascular dysfunction is emerging as a strong predictor of outcome in heart transplantation (HT). We assessed the validity of microvascular dysfunction, defined by means of a reduced coronary flow reserve (CFR), as a factor associated with new onset epicardial cardiac allograft vasculopathy (CAV) or death. We studied 105 patients at 4 ± 1 years post‐HT with a normal coronary angiography (CA). New onset CAV was assessed by CA. CFR was assessed in the left anterior descending (LAD) coronary artery by transthoracic Doppler echocardiography and calculated as the ratio of hyperaemic to basal blood flow velocity. A CFR ≤ 2.5 was considered abnormal. Epicardial CAV onset or death was assessed during a follow‐up of 10 years. New onset CAV was diagnosed in 30 patients (28.6%) (Group A), and the CA was normal in the remaining 75 patients (71.4%) (Group B). Group A had reduced CFR compared with group B (2.4 ± 0.6 vs. 3.2 ± 0.7, p < 0.0001). A CFR ≤ 2.5 was independently associated with a higher probability of new onset CAV (p < 0.0001) and a higher probability of death, regardless of CAV onset (p < 0.01). Microvascular dysfunction is independently associated with the onset of epicardial CAV, and associated with a higher risk of death, regardless of CAV onset.
Three-dimensional TEE is more accurate than 2DTTE and 2DTEE for determining LVOT and AA dimensions. When AS severity is determined by 3DTEE and corrected for PR using the 3D values, it needs to be reclassified from severe to moderate in almost a third of patients.
This study reveals that the finding of hemodynamically irrelevant PeEf in heart transplant patients is a predictor of adverse outcome, suggesting that a careful clinical assessment is warranted in heart transplant patients exhibiting small PeEf.
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