scholarly journals IN VIVO ESTIMATION OF MYOCARDIAL INFARCT SIZE AND LEFT VENTRICULAR FUNCTION BY PROSPECTIVELY GATED COMPUTERIZED TRANSMISSION TOMOGRAPHY

1983 ◽  
Vol 7 (6) ◽  
pp. 1134
Author(s):  
R. A. Slutsky ◽  
R. F. Mattrey ◽  
S. A. Long ◽  
C. B. Higgins
Keyword(s):  
Left Ventricular Function ◽  
Infarct Size ◽  
Ventricular Function ◽  
Myocardial Infarct ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
Transmission Tomography

Abstract 16538: Circulating Ketone Levels are Associated With Myocardial Infarct Size and Left Ventricular Function in Patients Presenting With St-Elevation Myocardial Infarction

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Marie Sophie L de Koning ◽  
B. D Westenbrink ◽  
Solmaz Assa ◽  
Dirk J van Veldhuisen ◽  
Robin P Dullaart ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ejection Fraction ◽  
Left Ventricular Function ◽  
Infarct Size ◽  
Ventricular Function ◽  
Myocardial Infarct ◽  
Left Ventricular ◽  
St Elevation Myocardial Infarction ◽  
Myocardial Infarct Size ◽  
St Elevation

Background: Circulating ketone bodies (KB) are increased in patients with heart failure, corresponding with increased utilization of KB as a cardiac fuel. Whether circulating KB are increased in patients presenting with ST-elevation myocardial infarction (STEMI) and whether this is associated with infarct size is unknown. Methods: KB were measured in 379 non-diabetic participants of the Glycometabolic Intervention as Adjunct to Primary Percutaneous Coronary Intervention in ST-Segment Elevation Myocardial Infarction (GIPS) III trial (Clinicaltrial.gov Identifier: NCT01217307). Non-fasting plasma concentrations of the KB beta-hydroxybutyrate, acetoacetate, acetone were measured at presentation, 24 hours and 4 months after STEMI presentation using nuclear magnetic resonance spectroscopy. Associations of circulating KB with myocardial infarct size and left ventricular ejection fraction (both detected with MRI at 4 months after STEMI) were determined using multivariable linear regression analyses. Results: Circulating KB were higher at baseline (total KB 520 [315-997](median [IQR], μmol/L), compared to 206 [174-246] at 24 hours and 166 [143-201] at 4 months ( P <0.001 for all)). KB at 24 hours were positively associated with enzymatic infarct size, HbA1C and beta-blocker use. KB at 24 hours were independently associated with MRI outcomes at 4 months. Higher KB was associated with larger myocardial infarct size (total KB: standardized β=0.17, 95%-confidence interval (CI) (0.04-0.31), P =0.012) and lower ejection fraction (standardized β=-0.15, 95%-CI (-0.29- -0.009), P =0.037). Conclusion: Circulating KB are increased in patients with STEMI and are independently associated with myocardial infarct size and left ventricular function after 4 months of follow-up. The increase in circulating KB may reflect maladaptive changes of myocardial metabolism during the acute phase.

Effect of levosimendan therapy on myocardial infarct size and left ventricular function after acute coronary occlusion

Heart ◽  
2016 ◽  
Vol 102 (6) ◽  
pp. 465-471 ◽  
Author(s):  
Miikka Tarkia ◽  
Christoffer Stark ◽  
Matti Haavisto ◽  
Rasmus Kentala ◽  
Tommi Vähäsilta ◽  
...  
Keyword(s):  
Left Ventricular Function ◽  
Infarct Size ◽  
Ventricular Function ◽  
Coronary Occlusion ◽  
Myocardial Infarct ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
Acute Coronary Occlusion

Voglibose, an Anti-diabetic Drug, Reduces Myocardial Infarct Size and Improves Left Ventricular Function in Rabbits

2007 ◽  
Vol 13 (6) ◽  
pp. S43
Author(s):  
Masamitsu Iwasa ◽  
Sinya Minatoguchi ◽  
Shouhei Sumi ◽  
Sinji Yasuda ◽  
Takahiko Yamaki ◽  
...  
Keyword(s):  
Left Ventricular Function ◽  
Infarct Size ◽  
Ventricular Function ◽  
Myocardial Infarct ◽  
Left Ventricular ◽  
Myocardial Infarct Size

The Effect Of Fibrinolysis In The Early Stage Of Acute Myocardial Infarction

1981 ◽  
Author(s):  
K Genth ◽  
J Frank ◽  
J Schaefer ◽  
V Korten ◽  
D Heene
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Ventricular Function ◽  
Early Stage ◽  
Myocardial Infarct ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
Time To Peak

The influence of streptokinase (SK) on myocardial infarct size and left ventricular function after acute myocardial infarction was investigated. 21 patients with myocardial infarction received SK (SK-group), 27 patients underwent conventional therapy (C-group). In both groups therapy started within 8 hours after onset of chest pain. In the SK-group initially 250 000 IU were administered intravenously, followed by a maintenance dose of 100 000 IU/h, lasting 15 hours. Blood samples at 8 hours intervals were collected for 3 days for serial CPK-analysis to calculate infarct size (I=∫f(t)×dt×K×bw). M-mode echocardiography was taken before start of t her a py and after 15, 24, 48 and 72 hours. AOP and heart rate were recorded continuously. Infarct size was 47±12g in the SK-group and 84±25g in the C-group (p<0.05). The average time to peak blood CPK-activity was 24 hours in the SK-group and 40 hours in the C-group. Peak CPK-level was significantly higher (p<0.5) in the SK-group (841±160U/l) than in the C-group (532±13 8 U / l ) . In 16 patients of the SK-group short periods of ventricular tachycardia were recorded during the period of fibrinolysis. Before therapy all patients showed abnormal motion of the posterior left ventricular wall and/or the interventricular septum, detected by echocardiography. 14 patients showed after fibrinolysis an improved or normalized motion.The results indicate that early fibrinolysis may reopen the occluded coronary artery. Reperfusion of the ischemic perfusion area may salvage jeo pardized myocardium, therefore infarct size was reduced and ventricular function improved.

Isoflurane Preconditions Myocardium Against Infarction via  Activation of Inhibitory Guanine Nucleotide Binding Proteins

2000 ◽  
Vol 92 (5) ◽  
pp. 1400-1407 ◽  
Author(s):  
Wolfgang G. Toller ◽  
Judy R. Kersten ◽  
Eric R. Gross ◽  
Paul S. Pagel ◽  
David C. Warltier
Keyword(s):  
Infarct Size ◽  
Pertussis Toxin ◽  
Myocardial Infarct ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
Area At Risk ◽  
Rate Of Increase ◽  
Gi Protein

Background Isoflurane-induced myocardial protection during ischemia is mediated by adenosine triphosphate-regulated potassium (KATP) channels; however, the intracellular signal transduction cascade responsible for this process has been incompletely evaluated. The authors tested the hypothesis that isoflurane reduces myocardial infarct size through a Gi protein-mediated process. Methods Forty-eight hours after pretreatment with vehicle (0.9% saline) or the Gi protein inhibitor pertussis toxin (10 microg/kg intravenously), barbiturate-anesthetized dogs (n = 43) were instrumented for measurement of aortic and left ventricular pressures and maximum rate of increase of left ventricular pressure. All dogs were subjected to a 60-min left anterior descending coronary artery occlusion followed by 3-h reperfusion. In four separate groups, vehicle- or pertussis toxin-pretreated dogs were studied with or without administration of 1 minimum alveolar concentration isoflurane. In two additional groups, dogs received the direct KATP channel agonist nicorandil (100 microg/kg bolus and 10 microg x kg-1 x min-1 intravenous infusion) in the presence or absence of pertussis toxin pretreatment. Myocardial perfusion and infarct size were measured with radioactive microspheres and triphenyltetrazolium staining, respectively. Results Isoflurane significantly (P &lt; 0.05) decreased infarct size to 7 +/- 2% of the area at risk compared with control experiments (26 +/- 2%). Pertussis toxin pretreatment alone had no effects on myocardial infarct size (31 +/- 4%) but blocked the beneficial effects of isoflurane (21 +/- 3%). Nicorandil decreased infarct size (11 +/- 2%), but, in contrast to isoflurane, this effect was independent of pertussis toxin pretreatment (11 +/- 1%). Conclusion Isoflurane reduces myocardial infarct size by a Gi protein-mediated mechanism in vivo.

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