Preinfarction Angina and Improved Reperfusion of the Infarct-related Artery

1999 ◽  
Vol 82 (S 01) ◽  
pp. 68-72 ◽  
Author(s):  
Alessandro Sciahbasi ◽  
Eugenia De Marco ◽  
Attilio Maseri ◽  
Felicita Andreotti
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Early Reperfusion ◽  
Vast Number ◽  
Beneficial Effects ◽  
Infarct Related Artery ◽  
Cardioprotective Effects ◽  
Collateral Vessels

SummaryPreinfarction angina and early reperfusion of the infarct-related artery are major determinants of reduced infarct-size in patients with acute myocardial infarction. The beneficial effects of preinfarction angina on infarct size have been attributed to the development of collateral vessels and/or to post-ischemic myocardial protection. However, recently, a relation has been found between prodromal angina, faster coronary recanalization, and smaller infarcts in patients treated with rt-PA: those with preinfarction angina showed earlier reperfusion (p = 0.006) and a 50% reduction of CKMB-estimated infarct-size (p = 0.009) compared to patients without preinfarction angina. This intriguing observation is consistent with a subsequent observation of higher coronary recanalization rates following thrombolysis in patients with prodromal preinfarction angina compared to patients without antecedent angina. Recent findings in dogs show an enhanced spontaneous lysis of plateletrich coronary thrombi with ischemic preconditioning, which is prevented by adenosine blockade, suggesting an antithrom-botic effect of ischemic metabolites. Understanding the mechanisms responsible for earlier and enhanced coronary recanalization in patients with preinfarction angina may open the way to new reperfusion strategies.A vast number of studies, globally involving ≈17,000 patients with acute myocardial infarction, have unequivocally shown that an infarction preceded by angina evolves into a smaller area of necrosis compared to an infarct not preceded by angina (Table 1) (1). So far, preinfarction angina has been thought to have cardioprotective effects mainly through two mechanisms: collateral perfusion of the infarctzone (2-4), and ischemic preconditioning of the myocardium (5-7). Here we discuss a further mechanism of protection represented by improved reperfusion of the infarct-related artery.

scholarly journals Cardioprotective Role of Colchicine Against Inflammatory Injury in a Rat Model of Acute Myocardial Infarction

2018 ◽  
Vol 23 (5) ◽  
pp. 446-455 ◽  
Author(s):  
Oussama Bakhta ◽  
Simon Blanchard ◽  
Anne-Laure Guihot ◽  
Sophie Tamareille ◽  
Delphine Mirebeau-Prunier ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Infarct Size ◽  
Messenger Rna ◽  
Transforming Growth Factor ◽  
Ischemia Reperfusion ◽  
Interleukin 1Β ◽  
Dependent Manner ◽  
Early Reperfusion ◽  
Beneficial Effects

Background: Inflammation plays a crucial role in the pathophysiology of myocardial ischemia/reperfusion (I/R) injury. A clinical trial has recently reported a smaller infarct size in a cohort of patients with ST-segment elevation myocardial infarction (MI) treated with a short colchicine course. The mechanism underlying colchicine-induced cardioprotection in the early MI phase remains unclear. We hypothesized that a short pretreatment with colchicine could induce acute beneficial effects by protecting the heart against inflammation in myocardial I/R injury. Methods and Results: Rats were subjected to 40-minute left anterior descending coronary occlusion, followed by 120-minute reperfusion. Colchicine (0.3 mg/kg) or a vehicle was administered per os 24 hours and immediately before surgery. Infarct size was significantly reduced in the colchicine group (35.6% ± 3.0% vs 46.6% ± 3.3%, P < .05). The beneficial effects of colchicine were associated with an increased systemic interleukin-10 (IL-10) level and decreased cardiac transforming growth factor-β level. Interleukin-1β was found to increase in a “time of reperfusion”-dependent manner. Colchicine inhibited messenger RNA expression of caspase-1 and pro-IL-18. Interleukin-1β injected 10 minutes prior to myocardial ischemia induced greater infarct size (58.0% ± 2.0%, P < .05) as compared to the vehicle. Colchicine combined to IL-1β injection significantly decreased infarct size (47.1% ± 2.2%, P < .05) as compared to IL-1β alone, while colchicine alone exhibited a significantly more marked cardioprotective effect than the colchicine-IL-1β association. Conclusion: The cardioprotection induced by a short colchicine pretreatment was associated with an anti-inflammatory effect in the early reperfusion phase in our rat MI model.

Captopril in acute myocardial infarction: Beneficial effects on infarct size and arrhythmias

1995 ◽  
Vol 18 (8) ◽  
pp. 465-470 ◽  
Author(s):  
Wulf-Dirk Bussmann ◽  
Guido Micke ◽  
Ralf Hildenbrand ◽  
Harald Klepzig
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Beneficial Effects

Calcium-Channel Blockers in Acute Myocardial Infarction

DICP ◽  
1989 ◽  
Vol 23 (7-8) ◽  
pp. 538-547 ◽  
Author(s):  
Michele F. Babich ◽  
Miriam L. Kalin ◽  
Donald C. Mcleod
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Left Ventricular ◽  
Channel Blockers ◽  
Beneficial Effects ◽  
Reinfarction Rate ◽  
Proper Patient Selection

The calcium-channel blockers are useful in treating a variety of cardiovascular disorders. Due to their antiischemic and spasmolytic properties, these agents have been studied in the prophylaxis and treatment of acute myocardial infarction. This article reviews this application with respect to reduction of mortality, infarct size, and reinfarction rate. Of the agents currently available for clinical use, nifedipine has been studied most extensively. This agent shows no beneficial effects in this setting and its use may in fact be harmful. Of the few trials that have been conducted with verapamil, none have shown decreased mortality. Verapamil may reduce infarct size although further confirmation is required. Diltiazem is the only agent that has been shown to have short- and long-term benefits in the patient with acute myocardial infarction. Proper patient selection is of utmost importance in ensuring successful therapy. In particular, those patients with non-Q-wave infarctions and/or normal left ventricular function can be expected to derive the most benefit in terms of reducing mortality and reinfarction rate associated with the acute event.

scholarly journals Exercise and Cardioprotection: A Natural Defense Against Lethal Myocardial Ischemia–Reperfusion Injury and Potential Guide to Cardiovascular Prophylaxis

2018 ◽  
Vol 24 (1) ◽  
pp. 18-30 ◽  
Author(s):  
Mohammed Andaleeb Chowdhury ◽  
Haden K. Sholl ◽  
Megan S. Sharrett ◽  
Steven T. Haller ◽  
Christopher C. Cooper ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Beneficial Effects ◽  
Natural Defense ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Similar to ischemic preconditioning, high-intensity exercise has been shown to decrease infarct size following myocardial infarction. In this article, we review the literature on beneficial effects of exercise, exercise requirements for cardioprotection, common methods utilized in laboratories to study this phenomenon, and discuss possible mechanisms for exercise-mediated cardioprotection.

Abstract 15656: Global Intracoronary Infusion of Allogeneic Cardiosphere-Derived Cells (CDCs) Immediately After Reperfusion Stimulates Myocyte Regeneration in Remote Viable Myocardium in Swine With Acute Myocardial Infarction

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Gen Suzuki ◽  
Brian R Weil ◽  
Merced M Leiker ◽  
Andrew Goelz ◽  
James A Fallavollita ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ejection Fraction ◽  
Infarct Size ◽  
Cell Size ◽  
Remote Myocardium ◽  
Viable Myocardium ◽  
Nuclear Density ◽  
Infarct Related Artery ◽  
Myocyte Proliferation

Introduction: Previous studies evaluating regenerative strategies have focused on administering stem cells to the infarct related artery. Unfortunately, this does not stimulate cardiac regeneration nor prevent myocyte loss in viable remote myocardium that becomes dysfunctional due to LV remodeling. Hypothesis: We hypothesized that administrating allogeneic CDCs to the entire heart (global CDC infusion) at the time of reperfusion could improve function, stimulate myocyte regeneration and prevent myocyte loss throughout the LV. Methods: Yorkshire swine (n=12) underwent a one hour LAD occlusion. Ejection fraction (EF) decreased from 63 ± 2% at baseline to 44 ± 2% after infarction (p<0.05 vs. baseline). Immediately after reperfusion animals were randomized to allogeneic intracoronary CDCs or vehicle in a blinded fashion (n=6 each). Allogeneic CDCs (20 x 10^6 CDCs, cyclosporine 100 mg/day) were infused into the 3 major coronary distributions without interrupting flow. Four weeks later we assessed myocardial function (echo), myocyte proliferation (Ki67), infarct size (TTC), myocyte nuclear density and cell size in comparison to vehicle. Results: After 4 weeks, global CDC infusion increased wall thickening and ejection fraction despite the fact that infarct volume was not different (Table). CDCs stimulated myocyte proliferation (Ki67) in border and remote regions by 3-fold. As a result, myocyte number (nuclear density) increased by 34 % and cell size decreased by 7% in viable infarct border and remote regions. Conclusion: Global infusion of allogeneic CDCs immediately after reperfusion 1.) stimulates myocyte regeneration in viable myocardium remote from the infarct and 2.) improves regional and global LV function without altering infarct size. Thus, treating viable remote myocardium as well as the infarct related artery with allogeneic CDCs may afford a widely available approach to reverse LV dysfunction in patients with acute myocardial infarction.

Beneficial Effects of Chronic Use of Aspirin and Nitrate on Infarct Size After Acute Myocardial Infarction

2013 ◽  
Vol 111 (7) ◽  
pp. 64B
Author(s):  
Doo Sun Sim ◽  
Young Keun Ahn ◽  
Myung Ho Jeong ◽  
Young Jo Kim ◽  
Shung Chull Chae ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Beneficial Effects ◽  
Chronic Use

Abstract 14058: Transvascular Total Left Ventricular Unloading for Acute Myocardial Infarction Strikingly Reduced Myocardial Oxygen Consumption, Limited the Infarct Size and Prevented Heart Failure in the long term

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Takahiro Arimura ◽  
Keita Saku ◽  
Takamori Kakino ◽  
Takuya Akashi ◽  
Yoshinori Murayama ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Oxygen Consumption ◽  
Infarct Size ◽  
Myocardial Oxygen Consumption ◽  
Left Ventricular ◽  
Early Reperfusion ◽  
The Impact

Backgrounds: Despite the latest progresses of early reperfusion, myocardial infarction (MI) remains a leading cause of chronic heart failure (CHF). Left ventricular (LV) assist device (VAD) mechanically unloads LV, thus myocardial oxygen consumption (MVO2). Theoretical analysis indicates that the partial VAD (p-VAD) where LV remains ejecting decreases preload (EDV) while increases afterload (ESV), thereby marginally decreases MVO2. In contrast, total LVAD (t-VAD) where LV no longer ejects, markedly decreases ESV as well as EDV, thus markedly reduces MVO2. We examined whether t-VAD in ischemia reperfusion (IR) could reduce the infarct size and prevent heart failure in the long term. Methods: First, in normal dogs, we examined the impact of p-VAD and t-VAD on MVO2 by Fick principle (coronary flow and arterial venous O2 difference). Second, we occluded the left anterior descending coronary artery for 3 hours and reperfused. We started transvascular LVAD (Impella®) from 1 hour after ischemia to 1 hour after reperfusion. We compared cardiac function, infarct size and hormones 1 month after ischemia among 3 groups, control group (IR, n=8), p-VAD (n=6), and t-VAD (n=6). Results: t-VAD markedly decreased MVO2 (p<0.05, Figure 1). 1 month after ischemia, t-VAD normalized LV end-systolic elastance (IR: 6.5±3.2, p-VAD: 9.7±1.3, t-VAD: 12.8±5.1 mmHg/ml, p<0.05) and reduced LV end-diastolic pressure (16.5±2.7, 6.4±2.9, 4.4±1.5 mmHg, p<0.05), and NT proBNP (3391±1364, 2084±348, 1632±228 pg/ml, p<0.05) indicating the successful prevention of heart failure. t-VAD markedly reduced the infarct size by more than 80% relative to IR (p<0.05, Figure 2) despite the fact that it started 1 hour after the onset of ischemia. Conclusions: Transvascular total left ventricular unloading for acute myocardial infarction strikingly reduces the MI size and prevents heart failure in the chronic phase. It might serve as a new therapeutic strategy in the management of patients with acute MI.

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