Myocardial infarction with and without reperfusion in sheep: early cardiac and neurohumoral changes

2000 ◽  
Vol 98 (6) ◽  
pp. 703-711 ◽  
Author(s):  
Christopher J. CHARLES ◽  
John M. ELLIOTT ◽  
M. Gary NICHOLLS ◽  
Miriam T. RADEMAKER ◽  
Mark RICHARDS
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Ejection Fraction ◽  
Troponin T ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Lv Function ◽  
Large Animal ◽  
Lv Dysfunction

There are few stable and reproducible large-animal models of chronic heart failure produced by ischaemic damage to the myocardium. Here we characterize a novel method of inducing myocardial damage in closed-chest sheep by catheter delivery of thrombogenic coils, and compare this with a newly described open-artery model of cardiac injury in sheep. Sham controls were compared with animals subjected to (a) 90 min of coronary artery occlusion/reperfusion by PTCA (percutaneous transluminal coronary angioplasty) balloon, and (b) permanent coronary artery occlusion induced by catheter delivery of thrombogenic coils (seven sheep/group). Both balloon occlusion/reperfusion and permanent coil occlusion resulted in well-defined anteroapical infarcts, as documented by ECG changes, significant rises in creatine kinase (both groups P < 0.001) and troponin-T (both groups P < 0.05), and post-mortem examination. Washout of enzymes was much more rapid in the reperfused group (P < 0.01). Infarction resulted in significant reductions in left ventricular (LV) ejection fraction (both groups P < 0.01) and regional wall abnormalities. Ejection fraction 7 days post-coil (21.3±4.2%) was significantly lower (P < 0.01) than that 7 days post-balloon (38.8±4.5%). Coil-induced infarction was associated with acutely reduced arterial pressure (P < 0.05), and increases in heart rate (P < 0.05), atrial pressures (P < 0.05), plasma brain natriuretic peptide levels (P < 0.05) and adrenaline levels (P < 0.05). Rises seen in plasma endothelin levels in sham controls were blunted in the coil group (P < 0.001). Haemodynamic changes were less marked in the balloon group. In conclusion, restriction of coronary artery occlusion to 90 min results in infarction, but less LV dysfunction with reduced early remodelling, compared with permanent occlusion. Acute changes in biochemical markers, haemodynamics, neurohormones and LV function confirm that these are excellent models of open- and closed-artery myocardial infarction leading to asymptomatic LV dysfunction.

scholarly journals Single-Point Cardiac Troponin T at Coronary Care Unit Discharge after Myocardial Infarction Correlates with Infarct Size and Ejection Fraction

2002 ◽  
Vol 48 (9) ◽  
pp. 1432-1436 ◽  
Author(s):  
Mauro Panteghini ◽  
Claudio Cuccia ◽  
Graziella Bonetti ◽  
Raffaele Giubbini ◽  
Franca Pagani ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ejection Fraction ◽  
Infarct Size ◽  
Cardiac Troponin ◽  
Coronary Care Unit ◽  
Troponin T ◽  
Left Ventricular ◽  
Lv Function ◽  
Cardiac Troponin T ◽  
Coronary Care

Abstract Background: One of the major concerns in replacing creatine kinase MB (CK-MB) with cardiac troponins is the lack of evidence of the ability of troponins to estimate the size of acute myocardial infarction (AMI). We investigated the ability of a single measurement of cardiac troponin T (cTnT) at coronary care unit (CCU) discharge to estimate infarct size and assess left ventricular (LV) function in AMI patients. Methods: We studied 65 AMI patients in whom infarct size was estimated by CK-MB peak concentrations and gated single-photon emission computed tomography (SPECT) myocardial perfusion using technetium-99m sestamibi and LV function by SPECT imaging. Measurements of cTnT and SPECT were performed 72 h (median) after admission (range, 40–160 h). SPECT was also repeated 3 months later. Results: We found a significant correlation between cTnT and both the peak CK-MB concentrations (r = 0.76; P &lt;0.001) and the perfusion defect size at SPECT (r = 0.62; P &lt;0.001). cTnT was inversely related to LV ejection fraction (LVEF) assessed both early (r = −0.56; P &lt;0.001) and 3 months after AMI (r = −0.70; P &lt;0.001). cTnT &gt;2.98 μg/L predicted a LVEF &lt;40% at 3 months with a sensitivity of 86.7%, specificity of 81.4%, and a likelihood ratio for a positive test of 4.7 (95% confidence interval, 4.0–5.4). Conclusions: A single cTnT measurement at CCU discharge after AMI is useful as a noninvasive estimate of infarct size and for the assessment of LV function in routine clinical setting.

Intermittent peripheral tissue ischemia during coronary ischemia reduces myocardial infarction through a KATP-dependent mechanism: first demonstration of remote ischemic perconditioning

2007 ◽  
Vol 292 (4) ◽  
pp. H1883-H1890 ◽  
Author(s):  
M. R. Schmidt ◽  
M. Smerup ◽  
I. E. Konstantinov ◽  
M. Shimizu ◽  
J. Li ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Ischemic Preconditioning ◽  
Limb Ischemia ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Force Frequency ◽  
Stroke Work ◽  
Dependent Mechanism

Remote ischemic preconditioning reduces myocardial infarction (MI) in animal models. We tested the hypothesis that the systemic protection thus induced is effective when ischemic preconditioning is administered during ischemia (PerC) and before reperfusion and examined the role of the K+-dependent ATP (KATP) channel. Twenty 20-kg pigs were randomized (10 in each group) to 40 min of left anterior descending coronary artery occlusion with 120 min of reperfusion. PerC consisted of four 5-min cycles of lower limb ischemia by tourniquet during left anterior descending coronary artery occlusion. Left ventricular (LV) function was assessed by a conductance catheter and extent of infarction by tetrazolium staining. The extent of MI was significantly reduced by PerC (60.4 ± 14.3 vs. 38.3 ± 15.4%, P = 0.004) and associated with improved functional indexes. The increase in the time constant of diastolic relaxation was significantly attenuated by PerC compared with control in ischemia and reperfusion ( P = 0.01 and 0.04, respectively). At 120 min of reperfusion, preload-recruitable stroke work declined 38 ± 6% and 3 ± 5% in control and PerC, respectively ( P = 0.001). The force-frequency relation was significantly depressed at 120 min of reperfusion in both groups, but optimal heart rate was significantly lower in the control group ( P = 0.04). There were fewer malignant arrhythmias with PerC during reperfusion ( P = 0.02). These protective effects of PerC were abolished by glibenclamide. Intermittent limb ischemia during myocardial ischemia reduces MI, preserves global systolic and diastolic function, and protects against arrhythmia during the reperfusion phase through a KATPchannel-dependent mechanism. Understanding this process may have important therapeutic implications for a range of ischemia-reperfusion syndromes.

Evolution of Scar Mechanical Properties During Myocardial Infarct Healing in Rat

2007 ◽  
Author(s):  
Gregory M. Fomovsky ◽  
Jeffrey W. Holmes
Keyword(s):  
Myocardial Infarction ◽  
Mechanical Properties ◽  
Rat Model ◽  
Important Determinant ◽  
Myocardial Infarct ◽  
Left Ventricular ◽  
Lv Function ◽  
Large Animal ◽  
Lv Dysfunction ◽  
Infarct Healing

The mechanics of healing myocardial infarcts are an important determinant of post-infarction left ventricular (LV) function and remodeling. Large animal infarct models are well studied; healing infarct scars have been shown to be mechanically and structurally anisotropic [1], and this anisotropy may help preserve LV function during some stages of healing [2]. At the same time, it has been suggested that the rat model of myocardial infarction is more similar to humans in the range of infarct sizes and observed LV dysfunction [3]. However, in the rat model, infarct mechanics and their effect on the overall LV function have not been described so far.

scholarly journals Myocardial infarction and ventricular fibrillation due to iatrogenic right coronary artery occlusion following tricuspid valve annuloplasty: a case report

2020 ◽  
Author(s):  
Shi Sum Poon ◽  
Joseph George ◽  
Daniel Obaid ◽  
Pankaj Kumar
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Tricuspid Valve ◽  
Right Coronary Artery ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Haemodynamic Instability ◽  
Tricuspid Valve Annuloplasty

Abstract Background Iatrogenic right coronary artery (RCA) injury is a rare complication of tricuspid valve annuloplasty. Given that surgical intervention is increasingly favoured for tricuspid regurgitation, it is of great importance to recognize potential complications following tricuspid valve surgery. Case summary A 72-year-old man underwent surgical mitral and tricuspid valve repair. The early post-operative course was complicated by recurrent ventricular fibrillation episodes. Due to haemodynamic instability, a re-sternotomy and another cardiopulmonary bypass run were required. The patient subsequently underwent coronary angiography study which confirmed RCA occlusion. The occluded posterior left ventricular (PLV) branch was reopened by balloon angioplasty. However, despite multiple attempts it was not possible to pass a coronary guide wire into the posterior descending artery (PDA). An intravascular ultrasound examination revealed that the ostium of the PDA was compressed by external factors leaving a narrow slit-like appearance with no accessible lumen. Subsequently, a drug-eluting stent was placed into the PLV branch. The PDA was not accessible on repeated re-canalization attempts. The patient later successfully recovered from the right ventricular myocardial infarction. Discussion Right coronary artery occlusion should be considered as a differential diagnosis for significant rhythm disturbances and haemodynamic instability in the peri- and post-operative period following tricuspid valve annuloplasty. A low threshold for diagnostic angiography is needed to avoid potential delay in life-saving revascularization.

Preoxygenated hemoglobin-based oxygen carrier HBOC-201 annihilates myocardial ischemia during brief coronary artery occlusion in pigs

2010 ◽  
Vol 298 (3) ◽  
pp. H1103-H1113 ◽  
Author(s):  
Maaike te Lintel Hekkert ◽  
Gregory P. Dubé ◽  
Evelyn Regar ◽  
Martine de Boer ◽  
Pascal Vranckx ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Stroke Volume ◽  
Reactive Hyperemia ◽  
Balloon Catheter ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Lv Function ◽  
Dependent Manner ◽  
Myocardial Oxygenation

Because of their ability to perfuse remote regions and deliver oxygen, hemoglobin-based oxygen carriers (HBOCs) may be considered in the treatment of several ischemic conditions such as acute coronary syndromes or high-risk percutaneous intervention. Here we studied the effects of intracoronary infusion of ex vivo preoxygenated HBOC-201 during brief total coronary artery occlusion (CAOs) on myocardial oxygenation and left ventricular (LV) function in a large animal model and investigated the influence of HBOC-201 temperature and infusion rate on these effects. Thirteen open-chest anesthetized swine were instrumented for measurement of global and regional LV function and metabolism. CAOs were induced by inflating an intracoronary balloon catheter; preoxygenated HBOC-201 (12 g/dL) was infused distally through the central lumen of the balloon catheter. Animals underwent consecutive 3-min CAOs interspersed by 30 min of reperfusion, accompanied by different HBOC-201 infusion rates (0, 15, 23, 30, 40, and 50 ml/min) and/or two infusion temperatures (18°C or 37°C) in random order. CAO elicited immediate loss of systolic shortening (SS) in the ischemic region (19 ± 1% at baseline vs. −3 ± 2% at end of CAO), resulting in decreases in maximum rate of rise in LV pressure (15 ± 5%) and stroke volume (12 ± 4%; all P < 0.05). Balloon deflation resulted in marked coronary reactive hyperemia (to 472 ± 74% of baseline), increases in coronary venous concentrations of adenosine + inosine (to 218 ± 26% of baseline; both P < 0.05) and rapid restoration of SS toward baseline. HBOC-201 ameliorated the CAO-induced changes in SS, stroke volume, reactive hyperemia, and coronary venous adenosine + inosine. The effects were temperature and flow dependent with full preservation of SS at 50 ml/min HBOC-201 of 37°C. In conclusion, intracoronary preoxygenated HBOC-201 preserved myocardial oxygenation and LV function in swine during CAO in a dose- and temperature-dependent manner. In our study setting, preoxygenated HBOC-201 can match the oxygen delivery role of endogenous blood in the heart on an almost equivalent-volume basis.

Blockade of AT1 receptors and Na+/H+exchanger and LV dysfunction after myocardial infarction in rats

1999 ◽  
Vol 277 (2) ◽  
pp. H610-H616 ◽  
Author(s):  
Marcel Ruzicka ◽  
Baoxue Yuan ◽  
Frans H. H. Leenen
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Cardiac Remodeling ◽  
Left Ventricular ◽  
Lv Function ◽  
Coronary Artery Ligation ◽  
Ang Ii ◽  
Artery Ligation ◽  
Volume Load ◽  
Lv Dysfunction

Mechanical stretch, ANG II, and α1-receptor stimulation may contribute to cardiac remodeling after myocardial infarction (MI). Each of these mechanisms involves different signaling pathways for the cellular hypertrophic response. All three also activate the Na+/H+exchanger. In the present study we evaluated the hypothesis that activation of the Na+/H+exchanger is involved in parallel with other signaling mechanisms for ANG II. Three days before coronary artery ligation, rats were randomly allocated to no treatment or treatment with amiloride, losartan, or amiloride and losartan in combination. Four weeks after coronary artery ligation, left ventricular (LV) function was assessed from in vivo resting cardiac pressures, hemodynamic responses to cardiac volume and pressure load, and cardiac remodeling by in vitro pressure-volume curves and LV and right ventricle (RV) weight. Amiloride and losartan given alone to a similar extent attenuated the shift of the pressure-volume curve to the right. This effect was significantly more pronounced with amiloride and losartan in combination. Each drug alone to a minor extent improved LV responses to pressure and volume load. However, with amiloride and losartan in combination, close-to-normal responses to pressure and volume load were observed. Losartan and amiloride alone had only a small effect on development of RV hypertrophy after MI but in combination completely prevented the RV hypertrophy. Amiloride and losartan appear to be complementary in prevention of cardiac remodeling and LV dysfunction after MI. This finding suggests that, besides ANG II, other mechanisms activating the Na+/H+exchanger contribute to cardiac remodeling after MI.

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