Phase Of Acute Coronary Occlusion Research Articles

Terapija poremećaja srčanog ritma u akutnom koronarnom sindromu

Acute myocardial infarction (AMI) is the worst acute syndrome of coronary heart diseases (CHD) with high morbidity and mortality, and it has become a serious threat to human health. A leading hypothesis for a major mechanism of arrhythmias in the acute phase of coronary occlusion is micro-reentry due to inhomogeneity of the electrical characteristics of ischemic myocardium. Arrhythmias could be of ventricular or supraventricular origin and the most often are: ventricular premature beats, accelerated idioventricular rhythm, ventricular tachycardia ventricular fibrillation and supraventricular premature beats and atrial fibrillation. Management of this arrhythmias consists not only of proper drug regime selection but also in their quick recognition or possible prediction and not less important, correction of variuos abnormalities such as: plasma electrolyte concentrations, acid-base balance disturbances, hypoxemia, anemia, and digitalis intoxication.

Acute proximal left anterior descending artery occlusion with de Winter sign

Prompt recognition of electrocardiographic signs of acute coronary occlusion is essential for timely restoration of flow. ST-segment elevation or new onset left bundle-branch block are the most common electrocardiographic changes seen in acute phase of coronary occlusion. However, some patients may present with atypical electrocardiographic signs, and early diagnosis of these patients may constitute a clinical challenge. Here, we report a 41-year-old man presenting with an atypical electrocardiographic manifestation despite angiographically confirmed acute thrombotic occlusion of proximal left anterior descending artery.

GW24-e0045 Assessment of Left Ventricular Regional Rotation in Early Phase of Acute Coronary Occlusion by Speckle Tracking Imaging

ObjectivesTo assess the left ventricular regional rotation of rabbit in early phase of acute coronary occlusion by speckle tracking imaging (STI), in order to investigate the sensibility of this method...

Abstract 5018: Soluble fms-like Tyrosine Kinase (sFLT1): A Biomarker of Endothelial Origin in Acute ST-segment Elevation Myocardial Infarction (STEMI)

In STEMI, early recognition improves clinical outcomes. Current biomarkers of myocardial necrosis are limited by poor sensitivity and specificity during the acute phase of coronary occlusion. sFLT1 is an endothelial-derived, hypoxia-inducible protein. We hypothesized that vascular occlusion induces early expression of sFLT1 in STEMI. Methods & Results: In a prospective, observational study, serum sFLT1 levels were measured by ELISA in 30 patients with STEMI referred for emergent catheterization. Compared to 20 healthy, age-matched controls, sFLT1 levels were markedly increased at the time of presentation (11.7±2 vs 210.5±80 pg/mL, p<0.0001), then substantially reduced within 24 hours of reperfusion (22.3±15 pg/mL, p<0.0001). On admission, 100% of STEMI patients had elevated sFLT-1 levels (>50pg/mL), whereas 73% and 64% had levels of CK-MB >5ng/mL and Troponin-I >1.0 ng/mL respectively. Two patients undergoing alcohol septal ablation were studied as positive controls. sFLT1 levels increased within 40 minutes of occlusion (27.8 vs 216.2 pg/mL, pre- vs post-ablation, p<0.03). We also studied sFLT1 expression in a mouse model of myocardial infarction (MI). After 1 hour of left coronary ligation in 10-week old male wild-type mice (n=6/group), left ventricular sFLT1 mRNA levels were increased (p<0.01 MI vs. sham), while aortic and lung mRNA expression were unchanged. Serum sFLT1 levels were also elevated in MI (170±71 vs 541±107pg/mL, sham vs. MI, p<0.002). To explore the cellular origin of sFLT1, human coronary endothelial (HCE) and smooth muscle cells (HSMC) were rendered hypoxic. Within 1 hour, sFLT1 mRNA expression in HCE increased by 173±35% (p=0.03). By 12 hours, sFLT1 mRNA and protein expression in hypoxic HCE increased by 313±15% (p<0.01) and 256±17% (p<0.001) respectively. To simulate the effects of reperfusion on sFLT1 expression, HCE were exposed to 12 hours of hypoxia, then 6 hours of normoxia. After normoxic rescue, sFLT1 protein expression decreased by 36% (p<0.01, vs hypoxic HCE). Hypoxia failed to induce sFLT1 mRNA or protein expression in HSMC. Conclusion: sFLT1 is a highly sensitive biomarker of vascular occlusion released by the endothelium during the acute phase of STEMI and may be an important new marker for acute ischemic syndromes. This research has received full or partial funding support from the American Heart Association, Founders Affiliate (Connecticut, Maine, Massachusetts, New Hampshire, New Jersey, New York, Rhode Island, Vermont).

Distinct modulation of angiotensin II-induced early left ventricular hypertrophic gene programming by dietary fat type

Long-term dietary fatty acid intake alters the development of left ventricular hypertrophy, but the linking signaling pathways are unclear. We studied the role and underlying signaling mechanisms of dietary fat intake in the early phase of the hypertrophic process. Rats assigned for 4 weeks of high-oil, high-fat, or standard diet were subjected to angiotensin II (Ang II; 33 microg/kg/h, subcutaneous) or vehicle infusion for 24 h. The Ang II-induced increase in left ventricular mRNA levels of hypertrophy-associated genes was higher in rats fed the high-oil diet compared with the standard diet. Western blotting revealed that, in parallel with changes in gene expression, the high-oil diet increased c-Jun N-terminal kinase phosphorylation (P < 0.001). Ang II increased p38 mitogen-activated protein kinase (MAPK) phosphorylation in rats fed the high-fat diet (3-fold; P < 0.01). The increase in transcription factor activator protein-1 (AP-1) DNA binding activity in response to Ang II was higher in rats fed the high-oil diet compared with those fed the standard diet (P < 0.001). Ang II downregulated inducible nitric oxide synthase mRNA levels in fatty acid-supplemented groups compared with the standard diet group. These results show that dietary fat type modulates the early activation of hypertrophic genes in pressure-overloaded myocardium involving the distinct activation of AP-1 and MAPK signal transduction pathways.

Diabetes and haemodynamic reactions to acute coronary occlusion

Background: The risk of early sudden death before hospital admission is higher in diabetic than non-diabetic men with acute myocardial infarction and autonomic nervous activity may modify the clinical outcome of abrupt coronary occlusion. Since diabetes mellitus may interfere with autonomic and myocardial function, we decided to study whether diabetes alters autonomic and haemodynamic responses to acute coronary occlusion. Methods: We analyzed the changes in heart rate, heart rate variability and blood pressure, and the occurrence of ventricular ectopy during a 2-min coronary occlusion in 238 non-diabetic and 32 diabetic patients referred for single vessel coronary angioplasty. The ranges of non-specific responses were determined by analyzing a control group of 19 patients with no ischaemia during a 2-min balloon inflation in a totally occluded coronary artery. Results: Diabetic patients were more often ( p<0.05) female, but there were no significant differences in the occluded vessel or incidence of ST changes or chest pain during coronary occlusion between the groups. Incidence of significant heart rate reactions and ventricular arrhythmias was comparable in both groups. Systolic blood pressure decreased ( p=0.01) in the diabetic patients during coronary occlusion, but did not change significantly in the non-diabetic group. Coronary occlusion caused more often (34% vs. 14%, p<0.01) a significant decrease in blood pressure in diabetic patients . Logistic regression models developed to analyze the significance of diabetes while controlling for baseline variables and signs of ischaemia identified diabetes to be an independent predictor of hypotensive reactions (odds ratio [OR] 2.9, 95% confidence intervals 1.1–7.8, p<0.05), while female gender and high short-term heart rate variability were other independent predictors of hypotensive reactions. Conclusions: Diabetic patients often develop significant hypotension during the early phase of acute coronary occlusion. This abnormality may be related to diabetic cardiomyopathy and impairment of baroreflex-mediated regulation of circulation. Predisposition to hypotension may contribute to the observed differences in the clinical presentation and outcome of acute coronary events.

Antiarrhythmic Effect of Magnolol and Honokiol during Acute Phase of Coronary Occlusion in Anesthetized Rats: Influence of L-NAME and Aspirin

This study was designed to evaluate the in vivo effect of magnolol and honokiol on the acute phase of coronary ligation in the presence of nitric oxide inhibitor (L-NAME) or cyclooxygenase inhibitor (aspirin). After Sprague-Dawley rats were anesthetized with urethane, the changes of ventricular arrhythmia induced by coronary ligation for 30 min were determined with or without pretreatment with study medications. The incidence and duration of ventricular arrhythmia were significantly reduced after intravenous pretreatment (15 min before coronary ligation) with 10^–7 g/kg magnolol or 10^–7 g/kg honokiol. However, the antiarrhythmic effect of magnolol or honokiol could be abolished with the pretreatment of 1 mg/kg L-NAME, but not with pretreatment of 100 mg/kg aspirin. The abolishment of the myocardial beneficial effect of magnolol and honokiol by L-NAME, instead of aspirin, suggests an involvement of an increased nitric oxide synthesis in the protection offered by magnolol and honokiol against arrhythmia during myocardial ischemia.

伸展活性化チャネルは急性冠閉塞直後の心電図変化と不整脈に関与する

伸展活性化チャネルは急性冠閉塞直後の心電図変化と不整脈に関与する

725-1 Long-term Impact of a Patent Infarct-related Artery: 1-Year Survival In the GUSTO Trial

The “open-artery” hypothesis has been validated in the acute phase of coronary occlusion. Controversy remains regarding long-term survival and the need for revascularization. To examine the long-term impact of a patent infarct-related artery in the GUSTO trial, we evaluated prospectively collected data on 41,021 patients treated with thrombolytic therapy for acute infarction. Patency data were available in 12,864 patients undergoing their first post-infarction angiogram who had no prior history of PTCA or CABG and who were not enrolled in the angiographic substudy. The infarct-related artery was open in 8,810 and closed in 4,054 patients. In the open artery cohort, 50% were treated medically, 38% with PTCA, and 12% with CABG. The corresponding percentages in the closed artery cohort were 45, 41 and 14, respectively. Baseline demographics, risk factor profiles, extent of disease and time to treatment were similar for both groups. Patients with a closed artery had a slightly higher incidence of Killip Class III and IV than the open artery cohort (2% vs 1%). As expected, patients treated medically and with PTCA in both groups had a preponderance of 1 and 2 vessel disease and patients treated with CABG had a preponderance of 2 and 3 vessel disease. 1-Year Mortality Open Artery Closed Artery P-value - Medical Therapy (%) 3.3 8.5 &lt;0.001 - PTCA(%) 2.5 88 &lt;0.001 - CABG(%) 4.2 9.6 &lt;0.001 Infarct-related artery patency confers a survival advantage at 1-year across all thrombolytic treatment strategies in patients with acute myocardial infarction.

Effect of propranolol on myocardial ischemia occurring during acute coronary occlusion.

In 16 patients undergoing angioplasty of the left anterior descending coronary artery, the clinical, electrocardiographic, and hemodynamic effects of short-term intravenous nonselective beta-adrenergic blockade with propranolol (0.1 mg/kg) were assessed during temporary occlusion of the artery. Myocardial ischemia during coronary occlusion was prevented, delayed in onset, or diminished in magnitude by propranolol in 10 of the 16 patients. Propranolol decreased values for indexes of myocardial oxygen demand, such as heart rate and blood pressure and their product, in all patients. Surprisingly, in patients who derived clinical benefit, propranolol did not change indexes of myocardial oxygen supply to the left ventricular region perfused by the occluded artery. For example, great cardiac vein flow (40 +/- 15 to 41 +/- 17 ml/min, p = NS) and coronary collateral resistance (2.1 +/- 1.0 to 2.1 +/- 1.1 mm Hg/ml/min, p = NS) were unchanged. In contrast, a worsening of supply occurred in patients who were not benefited: great cardiac vein flow (50 +/- 10 to 39 +/- 6 ml/min, p less than .05) decreased and coronary collateral resistance (1.6 +/- 0.5 to 2.0 +/- 0.6 mm Hg/ml/min, p less than .05) increased. Information obtained from this study demonstrates the value of this new experimental preparation in helping assess potential clinical effectiveness of drug interventions during the initial phase of acute coronary occlusion and providing insight into the mechanisms of drug effect.

Ventricular tachyarrhythmias induced by premature beats during acute coronary occlusion

Summary Ventricular tachyarrhythmias were induced in the ventricle during acute coronary occlusion by initiating closely coupled premature beats in the normal or ischemic areas. Acute coronary occlusion produced an initial decrease in the refractory period and conduction time in the affected area within about 3 min. of the start of coronary occlusion, followed by a subsequent increase in these parameters. Ventricular premature beats of the shortest coupling intervals could be initiated in the ischemic area during the initial phase of acute coronary occlusion when the refractory period was shortest, and these premature beats, in turn, induced ventricular tachyarrhythmias with an average time of 3 min 6 sec after the start of coronary occlusion. When the refractory period was subsequently increased in the ischemic area, ventricular premature beats of the shortest coupling intervals could be initiated in the normal area and these premature beats resulted in ventricular tachyarrhythmias with an average time of 7 min 10 sec after the start of coronary occlusion. The results indicate that ventricular premature beats initiated in the ischemic area are more likely to induce the tachyarrhythmias in the initial phase of acute coronary occlusion, while the premature beats initiated in the normal area are more likely to lead to ventricular tachyarrhythmias in the later stages of acute coronary occlusion.

A new therapeutic approach to acute coronary occlusion: I. Production of standardized coronary occlusion with microspheres

1. 1. A reproducible method for creating coronary occlusion with predictable and varied degrees of myocardial infarction in the closed chest animal is presented. 2. 2. Adjustment of microsphere dosage to animal body weight can provide animals suitable for study of the acute phase of coronary occlusion with high mortality or a preparation with myocardial infarction but long term survival suitable for the study of chronic coronary heart disease. 3. 3. Serum lactic dehydrogenase was observed to rise in all animals. The mean levels of response are directly related to microsphere dose and mortality. 4. 4. Two types of early death were observed in dogs that succumbed in 1 hour or less. Sixty per cent had shock followed by ventricular fibrillation in most cases. Forty per cent maintained an adequate blood pressure until ventricular fibrillation developed. Both mechanical failure and interruption of the normal conduction potential occurred in about equal proportions in the early deaths in this experiment. 5. 5. Electrocardiographic changes were inconsistent and sometimes transient in animals with proved disease at autopsy. 6. 6. Infarcts could be demonstrated in all dogs surviving 8 to 12 hours in this series. They closely approximated those in human subjects. Individual lesions could be found that were smaller than their human counterparts in those instances where coalescence of adjacent infarcts did not occur. 7. 7. Extracorporeal assisted circulation by arterioarterial counterpulsation has been previewed as a method of treating the early acute coronary occlusion.