scholarly journals Current Practice of Heart Donor Evaluation in Germany: Multivariable Risk Factor Analysis Confirms Practicability of Guidelines

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Sylke Ruth Zeissig ◽  
Carl-Ludwig Fischer-Froehlich ◽  
Frank Polster ◽  
Nils R. Fruehauf ◽  
Guenter Kirste ◽  
...  
Keyword(s):  
Organ Procurement ◽  
Left Ventricular ◽  
Organ Shortage ◽  
Logistic Regression Models ◽  
Donor Evaluation ◽  
Heart Donor ◽  
Severe Coronary Artery ◽  
Artery Disease ◽  
Donor Characteristics ◽  
First Time

Background. Organ shortage has liberalised the acceptance criteria of grafts for heart transplantation, but which donor characteristics ultimately influence the decision to perform transplantation? For the first time this was evaluated using real-time donor data from the German organ procurement organization (DSO). Observed associations are discussed with regard to international recommendations and guidelines.Methods. 5291 German donors (2006–2010) were formally eligible for heart donation. In logistic regression models 160 donor parameters were evaluated to assess their influence on using grafts for transplantation (random split of cases: 2/3 study sample, 1/3 validation sample).Results. Successful procurement was determined by low donor age (OR 0.87 per year; 95% CI [0.85–0.89],P<0.0001), large donor height (OR 1.04 per cm; 95% CI [1.02–1.06],P<0.0001), exclusion of impaired left ventricular function or wall motion (OR 0.01; 95% CI [0.002–0.036],P<0.0001), arrhythmia (OR 0.05; 95% CI [0.009–0.260],P=0.0004), and of severe coronary artery disease (OR 0.003; 95% CI [<0.001–0.01],P<0.0001). Donor characteristics differed between cases where the procedure was aborted without and with allocation initiated via Eurotransplant.

scholarly journals Dissociation of hemodynamic and electrocardiographic indexes of myocardial ischemia in pigs with hibernating myocardium and sudden cardiac death

2013 ◽  
Vol 304 (12) ◽  
pp. H1697-H1707 ◽  
Author(s):  
Matthew F. Pizzuto ◽  
Gen Suzuki ◽  
Michael D. Banas ◽  
Brendan Heavey ◽  
James A. Fallavollita ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Hibernating Myocardium ◽  
Sympathetic Activation ◽  
Premature Ventricular Contractions ◽  
Severe Coronary Artery ◽  
Artery Disease

Many survivors of sudden cardiac death (SCD) have normal global ventricular function and severe coronary artery disease but no evidence of symptomatic ischemia or infarction before the development of lethal ventricular arrhythmias, and the trigger for ventricular tachycardia (VT)/ventricular fibrillation (VF) remains unclear. We sought to identify the role of spontaneous ischemia and temporal hemodynamic factors preceding SCD using continuous telemetry of left ventricular (LV) pressure and the ECG for periods up to 5 mo in swine ( n = 37) with hibernating myocardium who experience spontaneous VT/VF in the absence of heart failure or infarction. Hemodynamics and ST deviation at the time of VT/VF were compared with survivors with hibernating myocardium as well as sham controls. All episodes of VT/VF occurred during sympathetic activation and were initiated by single premature ventricular contractions, and the VT degenerated into VF in ∼ 30 s. ECG evidence of ischemia was infrequent and no different from those that survived. Baseline hemodynamics were no different among groups, but LV end-diastolic pressure during sympathetic activation was higher at the time of SCD (37 ± 4 vs. 26 ± 4 mmHg, P < 0.05) and the ECG demonstrated QT shortening (155 ± 4 vs. 173 ± 5 ms, P < 0.05). The week before SCD, both parameters were no different from survivors. These data indicate that there are no differences in the degree of sympathetic activation or hemodynamic stress when VT/VF develops in swine with hibernating myocardium. The transiently elevated LV end-diastolic pressure and QT shortening preceding VT/VF raises the possibility that electrocardiographically silent subendocardial ischemia and/or mechanoelectrical feedback serve as a trigger for the development of SCD in chronic ischemic heart disease.

scholarly journals Impact of Arrhythmia on Myocardial Perfusion: A Computational Model-Based Study

Mathematics ◽  
2021 ◽  
Vol 9 (17) ◽  
pp. 2128
Author(s):  
Xinyang Ge ◽  
Sergey Simakov ◽  
Youjun Liu ◽  
Fuyou Liang
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Myocardial Perfusion ◽  
Myocardial Ischemia ◽  
Computational Model ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Metabolic Demand ◽  
Severe Coronary Artery ◽  
Artery Disease

(1) Background: Arrhythmia, which is an umbrella term for various types of abnormal rhythms of heartbeat, has a high prevalence in both the general population and patients with coronary artery disease. So far, it remains unclear how different types of arrhythmia would affect myocardial perfusion and the risk/severity of myocardial ischemia. (2) Methods: A computational model of the coronary circulation coupled to the global cardiovascular system was employed to quantify the impacts of arrhythmia and its combination with coronary artery disease on myocardial perfusion. Furthermore, a myocardial supply–demand balance index (MSDBx) was proposed to quantitatively evaluate the severity of myocardial ischemia under various arrhythmic conditions. (3) Results: Tachycardia and severe irregularity of heart rates (HRs) depressed myocardial perfusion and increased the risk of subendocardial ischemia (evaluated by MSDBx), whereas lowering HR improved myocardial perfusion. The presence of a moderate to severe coronary artery stenosis considerably augmented the sensitivity of MSDBx to arrhythmia. Further data analyses revealed that arrhythmia induced myocardial ischemia mainly via reducing the amount of coronary artery blood flow in each individual cardiac cycle rather than increasing the metabolic demand of the myocardium (measured by the left ventricular pressure-volume area). (4) Conclusions: Both tachycardia and irregular heartbeat tend to increase the risk of myocardial ischemia, especially in the subendocardium, and the effects can be further enhanced by concomitant existence of coronary artery disease. In contrast, properly lowering HR using drugs like β-blockers may improve myocardial perfusion, thereby preventing or relieving myocardial ischemia in patients with coronary artery disease.

Thirty-Five Day Impella 5.0 Support via Right Axillary Side Graft Cannulation for Acute Cardiogenic Shock

2013 ◽  
Vol 8 (4) ◽  
pp. 307-309 ◽  
Author(s):  
Mario A Castillo-Sang ◽  
Sunil M. Prasad ◽  
Jasvindar Singh ◽  
Gregory A. Ewald ◽  
Scott C. Silvestry
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Cardiogenic Shock ◽  
Artery Bypass ◽  
Complete Recovery ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Severe Coronary Artery ◽  
Artery Disease

We describe the use of an Impella 5.0 for mechanical support in acute cardiogenic shock after an acute myocardial infarction. A 61-year-old man with a history of severe coronary artery disease who underwent coronary artery bypass grafting with ischemic cardiomyopathy presented with cardiogenic shock after an ST-elevation myocardial infarction. An Impella Recover LP 5.0 (Abiomed, Danvers, MA USA) was inserted via a right axillary side graft, using transesophageal echocardiographic and fluoroscopic guidance. The patient remained in the intensive care unit, where he required a tracheostomy to beweaned off the ventilator. He required renal replacement therapy with subsequent complete recovery. His Impella support was weaned, and on postoperative day 35, the device was removed. The patient developed axillary thrombosis the morning after removal, requiring thrombectomy. Discharge echocardiogram showed mild left ventricular enlargement with global hypokinesis and left ventricular ejection fraction of 25%. The Impella 5.0 device can safely and effectively be used in the long-term support of cardiogenic shock.

scholarly journals Left Ventricular Chamber Volume, Mass, and Function in Severe Coronary Artery Disease

Circulation ◽  
1970 ◽  
Vol 41 (4) ◽  
pp. 605-613 ◽  
Author(s):  
CHARLES E. RACKLEY ◽  
H. DAVIS DEAR ◽  
WILLIAM A. BAXLEY ◽  
WILLIAM B. JONES ◽  
HAROLD T. DODGE
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Left Ventricular ◽  
Severe Coronary Artery Disease ◽  
Chamber Volume ◽  
Left Ventricular Chamber ◽  
Severe Coronary Artery ◽  
Artery Disease ◽  
And Function

Assessment of viability

2021 ◽  
pp. 545-564
Author(s):  
Luc A. Pierard ◽  
Paola Gargiulo ◽  
Pasquale Perrone-Filardi ◽  
Bernhard Gerber ◽  
Joseph B. Selvanayagam
Keyword(s):  
Coronary Artery ◽  
Myocardial Dysfunction ◽  
Oxygen Demand ◽  
Close Relation ◽  
Left Ventricular ◽  
Myocardial Oxygen Demand ◽  
Severe Coronary Artery ◽  
Coronary Syndromes ◽  
Artery Disease ◽  
Myocardial Thickening

Ischaemic left ventricular (LV) dysfunction due to coronary artery disease (CAD) is steadily increasing as a consequence of the ageing of the population and of improved survival of patients with acute coronary syndromes and currently represents the first cause of heart failure (HF). Myocardial function is dependent on blood supply, as anaerobic reserve is minimum due to a nearly maximal arteriovenous oxygen extraction. At rest, myocardial blood flow remains normal even in the presence of severe coronary artery stenosis (up to 85% diameter stenosis) by coronary autoregulation. In the presence of transstenotic pressure gradient due to epicardial coronary stenosis, arteriolar dilatation maintains normal myocardial flow at rest but with a progressive reduction in flow reserve. When arteriolar dilatation is maximal, autoregulation is exhausted and myocardial ischaemia develops. The limit of autoregulation depends on myocardial oxygen demand and is influenced by heart rate. Tachycardia increases oxygen demand and supply is reduced because of a decreased diastolic perfusion time. In the presence of acute ischaemia, there is a close relation between subendocardial perfusion and transmural function. Indeed, the contribution of subendocardium to myocardial thickening largely exceeds the contribution of the subepicardium. Akinesia can therefore result from subendocardial ischaemia and transmural ischaemia is not necessary. This chapter looks at how viability of the different techniques for treating myocardial dysfunction is assessed.

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