Development of cardiac allograft vasculopathy represents the major determinant of long-term survival in patients after heart transplantation. Due to graft denervation, these patients seldom present with classic symptoms of angina pectoris, and the first clinical presentations are progressive heart failure or sudden cardiac death. Although coronary angiography remains the routine technique for coronary artery disease detection, it is not sensitive enough for screening purposes. This is especially the case in the first year after transplantation when diffuse and concentric vascular changes can be easily detected only by intravascular ultrasound. The treatment of the established vasculopathy is disappointing, so the primary effort should be directed toward early prevention and diagnosis. Due to diffuse vascular changes, revascularization procedures are restricted only to a relatively small proportion of patients with favorable coronary anatomy. Percutaneous coronary intervention is preferred over surgical revascularization since it leads to better acute results and patient survival. Although there is no proven long-term advantage of drug-eluting stents for the treatment of in-stent restenosis, they are preferred over bare-metal stents. Severe vasculopathy has a poor prognosis and the only definitive treatment is retransplantation. This article reviews the present knowledge on the pathogenesis, diagnosis, treatment, and prognosis of cardiac allograft vasculopathy.
AimTo identify predictors of 3-month mortality after heart transplantation in a Croatian academic center.MethodsA retrospective review of institutional database identified 117 heart transplantations from January 2008 to July 2014. Two children <14 years were excluded from the study. The remaining 115 patients were dichotomized into survivors and non-survivors adjudicated at 3-months postoperatively, and their demographic, clinical, and longitudinal hemodynamic data were analyzed.Results3-month survival after heart transplantation was 86%. Non-survivors were older (59 ± 8 vs 50 ± 14 years, P = 0.009), more likely to have previous cardiac surgery (44% vs 19%; odds ratio [OR] 3.28, 95% confidence interval [CI] 1.08-9.90; P = 0.029), lower body mass index (BMI) (25 ± 4 vs 28 ± 2 kg/m2, P = 0.001), and be diabetics (44% vs 23%; OR 2.57, 95% CI 0.86-7.66; P = 0.083). Creatinine clearance was marginally superior among survivors (59 ± 19 vs 48 ± 20 mL/min, P = 0.059). Donor age and sex did not affect outcomes. Non-survivors were more likely to have had ischemic cardiomyopathy (69% vs 32%, P = 0.010). Postoperative utilization of epinephrine as a second line inotropic agent was a strong predictor of mortality (63% vs 7%; OR 21.91; 95% CI 6.15-78.06; P < 0.001). Serum lactate concentrations were consistently higher among non-survivors, with the difference being most pronounced 2 hours after cardiopulmonary bypass (9.8 ± 3.5 vs 5.2 ± 3.2 mmol/L, P < 0.001). The donor hearts exhibited inferior early hemodynamics in non-survivors (cardiac index 3.0 ± 1.0 vs 4.0 ± 1.1 L/min/m2, P = 0.001), stroke volume (49 ± 24 vs 59 ± 19 mL, P = 0.063), and left and right ventricular stroke work indices (18 ± 8 vs 30 ± 11 g/beat/m2, P < 0.001 and 5 ± 3 vs 7 ± 4 g/beat/m2, P = 0.060, respectively). Non-survivors were more likely to require postoperative re-sternotomy (50% vs 12%; OR 7.25, 95% CI 2.29-22.92; P < 0.001), renal replacement therapy (RRT) (69% vs 9%; OR 22.00, 95% CI 6.24-77.54; P < 0.001), and mechanical circulatory assistance (MCS) (44% vs 5%; OR 14.62, 95% CI 3.84-55.62; P < 0.001). Binary logistic regression revealed recipient age (P = 0.024), serum lactates 2 hours after CPB (P = 0.007), and epinephrine use on postoperative day 1 (P = 0.007) to be independently associated with 3-month mortality.ConclusionPretransplant predictors of adverse outcome after heart transplantation were recipient age, lower BMI, ischemic cardiomyopathy, reoperation and diabetes. Postoperative predictors of mortality were inferior donor heart hemodynamics, epinephrine use, and serum lactate concentrations. Non-survivors were more likely to require re-sternotomy, MCS, and RRT.
Some manufacturers do not provide automated intracardiac electrogram method (IEGM) systems for atrioventricular (AV) and interventricular (VV) delay optimization in cardiac resynchronization therapy (CRT). We aimed to evaluate the accuracy of manual IEGM method in 48 patients previously implanted with Medtronic Syncra CRT. All patients underwent standard device interrogation followed by CRT optimization by IEGM method and by echocardiography one month after implantation. The patient mean age was 60.7±11.8 years and there were 33 (68.8%) males. After CRT implantation, the left ventricular ejection fraction increased from 28.0±7.9% to 39.1±11.0% (p<0.001). Optimal aortic flow Velocity Time Integral (aVTI) was obtained when VV was set to 20-50 ms left ventricular pre-activation. There was a strong correlation between VV values determined by echocardiography and IEGM (R=0.823, p<0.001). We found no significant difference in AV, VV and aVTI values between echocardiography and IEGM method. However, IEGM was significantly less time-consuming than echocardiography [20 (10-28) vs. 40 (35-60) minutes, p<0.001]. Manual IEGM method may be good alternative to echocardiography and automated IEGM method. It also emphasizes the need for implementation of automated IEGM systems in as many CRT devices as possible.
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