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    Organ transplantation has kindled the human imagination since the beginning of time. Prehistorically, transplantation appeared as mythological stories: from creatures with body parts from different species, the heart transplant between two Chinese soldiers by Pien Ch’iao, to the leg transplant by physician Saints Cosmas and Damian. By 19th century, the transplantation concept become possible by extensive contributions from scientists and clinicians whose works had taken generations. Although Alexis Carrel is known as the founding father of experimental organ transplantation, many legendary names had contributed to the experimental works of heart transplantation, including Guthrie, Mann, and Demikhov. The major contribution to experimental heart transplantation before the clinical era were made by a team lead by Richard Lower and Norman Shumway at Stanford University in the early 1960s. They played the vital role in developing experimental and clinical heart transplantation as it is known today. Using Shumway biatrial technique Christiaan Barnard started a new era of clinical heart transplantation, by performing the first in man human-to-human heart transplantation in 1967. The techniques of heart transplant have evolved since the first heart transplant. This chapter will summarize the techniques that have been used in clinical heart transplantation.
    Creatures
    Human heart
    Citations (1)
    Abstract Background Re-worsening left ventricular ejection fraction (LVEF) after initial recovery occurs in some patients with dilated cardiomyopathy (DCM). However, prevalence and predictors of re-worsening LVEF in longitudinal follow-up are unclear. Late gadolinium enhancement of cardiovascular magnetic resonance (LGE-CMR) can evaluate the damage of myocardial tissue. Purpose This study sought to evaluate the clinical parameters including LGE-CMR to predict re-worsening LVEF in patients with recent-onset DCM. Methods We included patients with recent-onset DCM who had an LVEF <45% and underwent LGE-CMR at diagnosis. We performed yearly echocardiographc follow-up [median 6 [4–8.3] years]. Initial LVEF recovery defined as patients increased in >5% LVEF from baseline and had an LVEF≥45% after medical therapy. Patients were divided into three groups: (1) Improved: defined as those with sustained LVEF ≥45% after initial LVEF recovery; (2) Re-worse: those with decreased >5% and had an LVEF <45% after initial LVEF recovery. and (3) Not-improved: those with no initial LVEF recovery during follow-up. To evaluate the prognostic factors for Re-worsening LVEF after initial LVEF recovery, multivariate logistic regression analysis performed between the Improved group and the Re-worse group. Cardiac events defined as hospitalization due to heart failure and sudden death. Results Of 138 patents, 82 patients (59%) were the Improved group, 42 patients (30%) were the Re-worse group, and 14 (10%) were the Not-improved group. Loess curves of long-term LVEF trajectories showed that LVEF in the Re-worse group increased first 2 years and declined slowly thereafter (Fig. 1A). Re-worsening LVEF occurred 4.5±2.2 years after initial LVEF recovery. Multivariate logistic regression analysis demonstrated that LGE area at baseline (Odds ratio: 1.09, 95% confidence interval (CI) 1.02–1.18, p=0.014) and Log brain natriuretic peptide (BNP) at initial LVEF recovery (Odds ratio: 1.53, 95% confidence interval (CI) 1.01–2.31, p=0.042) were independent predictors for Re-worsening LVEF. Kaplan Meier analysis demonstrated that the risk of cardiac events in the Re-worse group was significantly higher (hazard ratio: 3.93, 95% CI 1.49–10.36, p=0.006) than in the Improved group and lower risk than in the Not-improved group (hazard ratio: 0.28, 95% CI 0.12–0.62, p=0.002) (Fig. 1B). Conclusion Re-worsening LVEF occurred in 30% of patients in patients with recent-onset DCM. LGE area and BNP at initial LVEF recovery were independently associated with re-worsening LVEF after initial LVEF recovery. Figure 1 Funding Acknowledgement Type of funding source: None
    Dilated Cardiomyopathy
    In 1905, Carrel and Guthrie reported the heterotopic heart transplantation on dogs for the first time. In the same year, Shone advanced the transplantation immunity theory which provided a basis for organ transplantation. In 1964, Hardy and his colleagues performed the first human chimpanzee heart transplantation. In 1967, Barnard performed the first human-to-human orthotopic heart transplantation in the world. In 1968 - 1971, 56 hospitals performed 180 heart transplantations world-wide. But because of the poor survival rate after operation, heart transplantations became less frequent. In 1972, Castaneda and Reitz summed up the experiences of heart-lung experimental transplantation, which laid a foundation for human heart-lung transplantation. In 1973, Caves invented myocardium biopsy for rejection surveillance after heart transplantation, which solved the problem of diagnosis for early rejection. In 1981, Stanford University first took cyclosporin A into clinical practice. The acute rejection after heart transplantation was effectively controlled and the long-term survival rate was significantly increased. Heart transplantation entered the second peak period. The launching of Asian heart transplantation began in 1968. Juro·Wada with his medical team performed the first heart transplantation in Japan. In 1978, Zhang Shize in Shanghai performed the first heart transplantation in China.
    Human heart
    Citations (1)
    To describe the impact of ejection fraction on the prognosis during 2 years after coronary artery bypass grafting (CABG).All patients in western Sweden who underwent CABG without concomitant valve surgery between June 1988 and June 1991.In all, 2121 patients were operated upon and information on ejection fraction was available for 1961 patients (92%). Of these patients, 178 (9%) had an ejection fraction < 40%, 517 (26%) an ejection fraction of 40-59% and 1266 (65%) an ejection fraction > or = 60%. In these groups the mortalities during the first 30 days after CABG were 5.1, 4.3 and 2.2%, respectively (P < 0.01). The corresponding values for mortalities between 30 days and 2 years were 7.7, 4.3 and 3.3%, respectively (P < 0.01). Patients with a lower ejection fraction were more frequently men and more frequently had a history of cardiovascular disease. In multivariate analysis the preoperative ejection fraction was an independent predictor for total 2-year mortality. Patients with a low ejection fraction died more frequently in association with ventricular fibrillation. Morbidity was, with the exception of that for rehospitalization due to heart failure and infection, not associated significantly with the preoperative ejection fraction.During the 2 years after CABG a low preoperative ejection fraction was associated with a higher mortality, but the association with morbidity was more complex.
    Concomitant
    Background: A significant proportion of patients diagnosed as heart failure have preserved ejection fraction. However, the differentiation between heart failure with reduced & preserved ejection fraction is difficult. Method: The medical records of young patients (20–40 years) admitted during the two years 2014 & 2015 and diagnosed with Heart Failure were scrutinized in an attempt to determine the proportion of patients with preserved vs reduced ejection fraction and to assess the relationship between their Brain-type Natriuretic Peptide (BNP) levels & Left Ventricular Ejection Fraction (LVEF) in both the groups. Results: After Statistical analysis, it was found that around 36% of heart failure patients had preserved ejection fraction. There was a negative correlation between BNP levels & LVEF in both heart failure with reduced ejection fraction (HFrEF) as well as that with preserved ejection fraction (HFpEF). Majority of patients in HFpEF group were females. Mean BNP level in HFpEF group was significantly lower than that in the HFrEF group. Conclusion: Around one third of patients had Heart Failure with preserved systolic function, of which majority are females. There is a strong negative correlation between BNP levels and LVEF% in both the groups. Thus. BNP levels can be used in the differentiation of HFpEF and HFrEF. Keywords: Heart Failure, BNP levels, LVEF, Preserved & reduced ejection fraction
    Brain natriuretic peptide
    Citations (0)
    Background: A significant proportion of patients diagnosed as heart failure have preserved ejection fraction. However, the differentiation between heart failure with reduced & preserved ejection fraction is difficult. The objectives of the study include: To assess the BNP levels in both patients with Heart failure with preserved LV ejection fraction and those with reduced LV ejection fraction. To study the correlation between the BNP levels and LVEF in both the groups and to ascertain whether BNP can be an useful tool in diagnosis of Heart failure with preserved LV ejection fraction]. Methods: The medical records of young patients (20–40 years) admitted during the two years 2014 & 2015 and diagnosed with Heart Failure were scrutinized in an attempt to determine the proportion of patients with preserved vs reduced ejection fraction and to assess the relationship between their Brain-type Natriuretic Peptide (BNP) levels & Left Ventricular Ejection Fraction (LVEF) in both the groups.  Results: After Statistical analysis, it was found that around 36% of heart failure patients had preserved ejection fraction. There was a negative correlation between BNP levels & LVEF in both heart failure with reduced ejection fraction (HFrEF) as well as that with preserved ejection fraction (HFpEF). Majority of patients in HFpEF group were females. Mean BNP level in HFpEF group was significantly lower than that in the HFrEF group.  Conclusion: Around one third of patients had Heart Failure with preserved systolic function, of which majority are females. There is a strong negative correlation between BNP levels and LVEF% in both the groups. Thus BNP levels can be used in the differentiation of HFpEF and HFrEF.
    Brain natriuretic peptide