Complete Coronary Artery Occlusion Research Articles

The relationship between mechanical dyssynchrony of the left ventricular myocardium and the degree of coronary artery occlusion in patients with coronary artery disease

Background. The prevalence of chronic heart failure in the world is increasing; however, it is stabilizing in developed countries. One of the reasons for this stabilization is an improvement of acute coronary syndrome treatment and revascularization. Revascularization in patients with chronic coronary syndromes without signs of the left ventricular dysfunction is less effective. One of the promising methods for assessing left ventricular dysfunction is the detection of electrical and mechanical dyssynchrony of the myocardium (DM). However, mechanical dyssynchrony of the myocardium has not been sufficiently studied in patients with coronary artery (CA) disease. The purpose was to assess the relationship between mechanical myocardial dyssynchrony and the degree of coronary artery occlusion in patients with coronary artery disease who underwent revascularization. Materials and methods. One hundred and thirty-four patients with coronary artery disease (35 with myocardial infarction and 99 with chronic coronary syndromes) who underwent coronary angiography and revascularization of coronary arteries were included in the study. According to the results of coronary angiography, patients were divided into 3 groups: 12 had unchanged CA (group 1), 17 had atherosclerotic lesions of CA without signs of occlusion (group 2), and 105 patients were with CA occlusion. Among those with CA occlusion, 10 people had an occlusion of less than 50 %, 26 patients had occlusion from 50 to 80 %, 36 had more than 80 %, and 33 patients had complete occlusion of at least one coronary artery. In all patients, parameters of mechanical DM were determined by ultrasound method. Results. In the first group, 3 patients (25 %) had mechanical DM, in the second — 4 patients (23.5 %), in the group with coronary artery occlusion, 42 patients (40 %) had mechanical DM. In the group with complete CA occlusion, mechanical DM was detected in 18 (53 %) cases. Septal to posterior wall motion delay (SPWMD) did not differ significantly in the comparison groups; however, it increased significantly to 64.8 ± 43.2 ms in patients with complete CA occlusion compared with 40.8 ± 13.1 ms in the group with unchanged CA (p < 0.05). SPWMD had a significant correlation with the degree of CA occlusion (r = 0.254, p = 0.009). The interventricular mechanical delay increased significantly, to 61.3 ± 40.5 ms compared with 33.4 ± 3.4 ms in patients with unchanged CA (p < 0.05). Left ventricular filling time was significantly shorter in the group with complete CA occlusion compared to the patients with incomplete CA occlusion and those with unchanged CA (47.3 ± 10.4 ms vs. 54.2 ± 5.7 ms, respectively; p < 0.05). Left ventricular ejection time was not significantly different between comparison groups, but correlated significantly with the degree of CA occlusion (r = 0.241, p = 0.013). The early ventricular time deceleration, the time from the beginning of the QRS complex to the beginning of the peak systolic velocity did not differ significantly. The time to the peak systolic velocity was significantly longer in the group with complete CA occlusion (32.6 ± 8.5 ms), and had a significant correlation with the degree of CA occlusion (r = 0.26, p = 0.007). Conclusions. A third of patients with chronic coronary syndrome included in the study had DM. In the group with complete CA occlusion, the frequency of DM detection increased significantly and was diagnosed in half of cases. In patients with complete CA occlusion, DM manifested itself in a significant SPWMD, an increase in the period of pre-ejection into the aorta and, as a result, a significant increase in the interventricular mechanical delay. An increase in the time to peak systolic velocity was also found in the group of patients with complete CA occlusion. DM associated with left ventricular diastolic dysfunction was detected in a group of patients with complete CA occlusion and manifested itself in a reduced left ventricular filling time.

H-type hypertension is a risk factor for chronic total coronary artery occlusion: a cross-sectional study from southwest China

BackgroundChronic total coronary occlusion (CTO) is serious and the "last bastion" of percutaneous coronary intervention. Hypertension and hyperhomocysteinemia (HHCY) are synergistic and significantly increase cardiovascular event risk. The relationship between H-type hypertension and CTO remains unclear; thus, this cross-sectional study investigated this potential association.MethodsBetween January 2018 and June 2022, 1446 individuals from southwest China were recruited to participate in this study. CTO was defined as complete coronary artery occlusion persisting for over three months. H-type hypertension was defined as hypertension with plasma homocysteine levels ≥ 15 µmol/L. Multivariate logistic regression models were applied to assess the association between H-type hypertension and CTO. Receiver operating characteristic (ROC) curves were generated to determine the accuracy of H-type hypertension in predicting CTO.ResultsOf the 1446 individuals, 397 had CTO, and 545 had H-type hypertension. After multivariate adjustment, the odds ratio (OR) for CTO in individuals with H-type hypertension was 2.3-fold higher (95% CI 1.01–5.26) than that in healthy controls. The risk of CTO is higher in individuals with H-type hypertension than in those with isolated HHCY and hypertension. The area under the ROC curve for CTO was 0.685 (95% CI, 0.653–0.717) for H-type hypertension.ConclusionsIn southwest China, H-type hypertension is significantly related to the occurrence of CTO.Trial registrationThis retrospective study was registered with the Chinese Clinical Trials Registry (http://www.chictr.org.cn, ChiCTR2100050519.2.2).

Copeptin levels as a predictor of acute kidney injury (AKI) in ST-segment elevation myocardial infarction (STEMI)

Background: Acute myocardial infarction is a cardiac emergency with a high mortality rate. The ST-segment elevation myocardial infarction (STEMI) patients have complete coronary artery occlusion, so they usually present with severe symptoms and a higher risk of early mortality. The prevalence of type 1 cardiorenal syndrome (CRS), namely acute kidney injury (AKI) in acute heart failure, is 24%-45%. Copeptin is the C-terminus of pro-vasopressin's peptide, the arginine vasopressin's precursor. This study aimed to prove whether copeptin is a predictor of AKI in the STEMI patient population after adjusting for confounding variables. Methods: This prospective cohort study was conducted between March and December 2020. Eighty-four subjects with STEMI who came to the emergency department at Dr. Moewardi Hospital and met the inclusion and exclusion criteria were enrolled. The data were analyzed to calculate relative risk and 95%CI for each variable, followed by multivariate analysis with logistic regression. Data were analyzed using SPSS version 23 for Windows. Results: The prevalence of AKI in this study was 67%. The copeptin level at the cut-off of 273.6 pg/ml has an AUC of 0.774 (95%CI=0.676-0.873, p=0.000). Copeptin level, acute heart failure, and risk of renal ischemia associated with AKI in STEMI. Copeptin >273.6 pg/ml showed a statistically significant association with AKI in STEMI (adjusted RR 5.298; 95%CI=1.771-15.847; p=0.003). Conclusion: Copeptin levels higher than 273.6 pg/ml is known to be an independent predictor of AKI in STEMI.

Течение инфаркта миокарда у женщин трудоспособного возраста

The incidence of myocardial infarction (MI) among women of working age has continued to grow in recent years, being a great socio-economic problem. The purpose — to study the features of MI course in women under the age of 60. Results. The following risk factors were identified: hyperlipidemia (74.2%), arterial hypertension (AH) (69.4%), smoking (35.5%), obesity (37.1%), and diabetes mellitus (DM) (29.0%). Hyperuricemia (HU) occurred in 38.7% of patients. Repeated MI was observed in 3.2% of patients. Anterior and lower MI occurred with approximately the same frequency (45.2% and 40.3%, respectively). The percentage of coronary artery (CA) lumen stenosis was 81.2 ± 19.6%. Thrombosis with complete CA occlusion was detected in 61.3%. The percentage of brachiocephalic artery (BCA) lumen stenosis was 21.5 ± 7.5%. Thickness of the intima-media complex (TIMC) of BCA in the carotid artery bifurcation zone was 1.1 ± 0.2 mm on the right and 1.1 ± 0.2 mm on the left. We revealed a direct correlation between the level of uric acid (AU) and TIMC BCA (correlation coefficient 0.36; p ˂ 0.05) and an inverse correlation between the UA values and the glomerular filtration rate (GFR) (correlation coefficient 0.36; p ˂ 0.05), which indicates the important role of HU. Conclusions. Among the risk factors of MI development in women under 60 years of age, hyperlipidemia, hypertension, smoking, HU and DM are of the greatest importance. Hemodynamically significant stenosis was only in CA, multifocal atherosclerosis was not detected. HU is the most important factor of MI development in women. It has a negative effect on BCA and GFR and increases the likelihood of a brain stroke. It is necessary to include UA in the standards of examination of all forms of coronary heart disease. In case of a high cardiovascular risk, it should be reduced to the target level below 360 mmol/l to prevent cardiovascular complications.

Influence of circadian rhythms and seasonal and annual variations on acute myocardial infarction incidence

Background/Aim: Acute myocardial infarction (AMI) is a consequence of complete coronary artery occlusion. There is a considerable seasonal variation in the incidence of AMI. The aim of the study was to establish a circadian and seasonal pattern of AMI. Methods: A retrospective observational study was conducted, using the database of the Institute of Emergency Medical Service of the City of Novi Sad. The study included 982 patients, both male and female, diagnosed with AMI (I.21 - ICD-10 code) in the period between 15 March 2018 and 14 March 2022. Data were classified according to the time of the day, days of the week, quarters and months. Data were analysed by using descriptive statistical methods, Mann-Whitney U test, Chi-squared test and Fisher's exact test. Results: AMI most frequently occurred between 6 am and 2 pm (389; 39.6 %). A statistically significant incidence of AMI was calculated for the periods between 6 am and 2 pm (ch2 = 39.69; p < 0.001) and between 2 pm and 10 pm (ch2 = 28.06; p < 0.001). Most cases of AMI were noted on Monday (153; 15.6 %) and in January (93; 9.5 %). The highest incidence of AMI was in the period between 15 March 2021 and 14 March 2022 (304; 31.0 %), while the lowest incidence was noted between 15 March 2019 and 14 March 2020 (190; 19.3 %). Conclusion: Circadian, seasonal and annual rhythm may have a significant impact on the incidence of AMI. This fact can have an important role in the prevention, timely recognition and adequate treatment of acute coronary disease.

Wellens Syndrome on the basis of critical occlusion of the medial segment of the anterior ventricultural branch of the left coronary artery (clinical type)

The aim of the work is to determine the peculiarities of the clinical course of Wellens syndrome due to the presence of critical occlusion of the medial segment of the anterior interventricular coronary artery bifurcation.Material and Methods. Clinical manifestations of the disease, including dynamics of ECG changes; coronary angiography data; results of echocardiographic and laboratory tests.Results. This article presents the peculiarities of the clinical course of Wellens syndrome in patient L., 70, who met the currently recognized diagnostic criteria of the syndrome, but the critical occlusion of the anterior interventricular branch of the left coronary artery was localized in its medial segment. Along with this, there was hemodynamically irrelevant stenosis of the proximal coronary artery section (60%). Electrocardiographic changes were consistent with pattern B (deeply inverted T waves in V2-V6). Сonditional normalization of the T waves, indicating the absence of repeated coronary artery occlusion after spontaneous reperfusion. Stenting of the anterior interventricular coronary artery vein of the left coronary artery prevented the possible occurrence of “stuttering” pattern and the occurrence of myocardial infarction.Conclusions. Acute coronary syndrome with complete coronary artery occlusion is often accompanied by spontaneous reperfusion, which contributes to the relief of chest pain and the appearance of characteristic T waves on ECG and is the basis of the so-called Wellens syndrome. The most frequent localization of coronary artery occlusion is the proximal segment of the anterior interventricular branch of the left coronary artery, but we witnessed the occlusion in the medial segment of these coronary arteries. Immediate coronary angiography with stenting of the occluded artery will prevent the occurrence of myocardial infarction in the patient.

Meta-analysis on efficacy of PCI treatment or conservative treatment among patients with chronic total occlusions

Objective: To compare the efficacy between percutaneous coronary intervention (PCI) and conservative medication treatment in chronic total occlusions (CTO) patients. Methods: It was a meta-analysis.Articles on drug therapy and PCI for complete coronary artery occlusion were retrieved from Pubmed, Embase and Web of Science databases. The search time was from the database construction to May 10, 2020, and the following search criteria were used for the search "chronic total occlusion" "percutaneous coronary intervention" and "medical therapy". References from searched literatures were also searched to identify more eligible studies. Randomized controlled trials (RCT) and cohort studies comparing efficacy of PCI versus oral medication as well as medication as initial therapy option for CTO patients with single or multiple lesions were included. The primary endpoints included all-cause death, cardiac death, recurrent myocardial infarction, re-revascularization, major adverse cardiac events (MACE) and stroke. Data were analyzed with ReviewManager5.3.0 software. Pooled effect size RR and 95%CI were calculated by randomization effect model. Heterogeneity was evaluated by I2. Bege test was used to evaluate publication bias. Subgroup analyses were performed for RCT and cohort studies. Results: A total of 1 079 articles were retrieved and 16 studies (RCT=4, cohort study=12) were included with 12 223 patients. Fourteen publications (RCT=4, cohort study=10) reported all-cause death post PCI and/or drug therapy. Results showed that risk of all-cause death was significantly lower in PCI group than in drug therapy group (RR=0.45,95%CI 0.39-0.53,P<0.001);subgroup analysis showed that risk of all-cause death was significantly lower in PCI group than in drug therapy group from cohort studies (RR=0.44,95%CI 0.38-0.52,P<0.001),but comparable in RCT (P=0.27). Thirteen studies (RCT=3, cohort study=10) reported cardiac death post PCI and/or drug therapy. Results showed that risk of cardiac death was significantly lower in PCI group than in drug therapy group (RR=0.44,95%CI 0.35-0.55,P<0.001);subgroup analysis showed that risk of cardiac death was significantly lower in PCI group than in drug therapy group in cohort studies (RR=0.43,95%CI 0.34-0.54,P<0.001),but not in RCT (P=0.25). Fourteen publications (RCT=4, cohort study=10) reported recurrent myocardial infarction post PCI and/or drug therapy. Results showed that risk of recurrent myocardial infarction was significantly lower in PCI group than in drug therapy group (RR=0.62,95%CI 0.44-0.88,P=0.007);subgroup analysis showed that risk of recurrent myocardial infarction was significantly lower in PCI group than in drug therapy group from cohort studies (RR=0.56,95%CI 0.40-0.78,P=0.000 5),but comparable in RCT (P=0.17). Fourteen publications (RCT=4, cohort study=10) reported re-revascularization post PCI and/or drug therapy. Results showed that risk of re-revascularization was comparable between PCI group and drug therapy group (P=0.91);subgroup analysis showed that risk of re-revascularization was comparable between PCI group and drug therapy group both in cohort study and RCT (P=0.60 and 0.41, respectively). Eleven publications (RCT=3, cohort study=8) reported MACE post PCI and/or drug therapy. Results showed that risk of MACE was significantly lower in PCI group than in drug therapy group (RR=0.74,95%CI 0.59-0.93,P=0.03);subgroup analysis showed that risk of MACE was significantly lower in PCI group than in drug therapy group in cohort studies (RR=0.72,95%CI 0.56-0.93,P=0.01), but not in RCT (P=0.8). Six publications (RCT=2, cohort study=4) reported stroke post PCI and/or drug therapy. Results showed that risk of stroke was comparable between PCI and drug therapy groups (RR=0.62,95%CI 0.32-1.20, P=0.15);subgroup analysis showed that risk of stroke was comparable between PCI and drug therapy groups both in cohort studies and RCT (P=0.48 and 0.32, respectively). Conclusion: Compared with oral drug therapy, PCI may have better efficacy for CTO patients based on results from this cohort study.

PO-626-07 VALIDATION OF A PORTABLE DEVICE FOR HF-ECG IN ISCHEMIA DETECTION DURING CORONARY BALLOON INFLATION IN ANGIOPLASTY - BRINGING THE PHYSIOLOGY LAB TO THE BEDSIDE !

High frequency QRS (HfQRS) analysis for rapid assessment of myocardial ischemia has never been evaluated owing to the logistical challenges of signal recording. We aim to evaluate, in a pilot study, the correlation between the HFQRS changes recorded on a novel wearable Sydäntek 12 lead ECG patch with balloon inflation induced ischaemia. To document utility of a portable device, Sydäntek, in ECG and HFECG during multiple balloon inflations. 10 patients (M:F = 8:2) undergoing coronary intervention for medically refractory chronic stable angina were screened for enrollment into the study ; 9/10 patients underwent the final recording. 1 patient was excluded owing to signal noise in the device due to reluctance in chest preparation. The mean recording time per case was 60+/-15 mins. ECG including HfQRS was recordable continuously during all intended times, using Sydäntek at 2k samples/secs. In 33 balloon inflation ischemia episodes , changes were seen on the HFQRS onset ∼ 10 secs, offset ∼45 secs after deflation . No significant changes were seen in the conventional ECG analysed for these upto ∼45 secs . Decrease in the amplitude of the HFQRS, and decrease in the real time RMS voltage of QRS in leads V2-V5 and the presence of RAZ ( reduced amplitude zone ) were considered to be changes suggestive of ischemia. RAZ disappeared ∼45 secs after the balloon deflation. The mean total ischemic was 1 +/-0.5 min per patient per balloon inflation. In this study , all 9 of the conventional ECGs were reported independently by 2 docs as not having significant ST-T changes of ischaemia. RAZ presence in HFQRS was seen in all 33 of complete coronary artery occlusion by balloon, in our study .There was reduction in the amplitude of HFQRS(mean 12+/-1 μV) and RMSv2-v5 (mean 7+/-0.5 μV) from the baseline during the inflation. Post intervention, both of the above parameters had a mean increase of 22+/-1 μV and 10+/-0.3 μV respectively. HFQRS measured using our novel, portable real time 12 lead ECG recording patch can reliably detect onset of coronary ischemia in a complete coronary occlusion even in absence of ST -T changes in 12 lead ECG . We submit this proof of concept for use in detecting ischemia in a variety of clinical situations including chest pain triage and post intervention monitoring.

Effect of late culprit coronary artery revascularization on prognosis of patients with ST-elevation myocardial infarction

Aim. To evaluate the effect of culprit coronary artery revascularization after 48 hours from the symptoms’ onset on the prognosis of patients with ST-elevation myocardial infarction (STEMI).Material and methods. Of the 1172 patients admitted to City Clinical Hospital № 13 in 2018 due to STEMI, 43 patients (4%) were included in the retrospective study. There were following inclusion criteria: hospitalization after 48 hours from the symptoms’ onset, no clinical signs of myocardial ischemia, and complete coronary artery occlusion according to angiography. The mean age of the subjects was 61,3±10,6 years, 34 (79%) men and 9 (21%) women. The subjects were divided into two groups: group 1 (n=22) — management with percutaneous coronary intervention (PCI), group 2 (n=21) — management with medications. The groups differ only in the severity of coronary atherosclerosis according to SYNTAX score: group 1 — 14,0 [11.0; 19.5], group 2 — 26,0 [16,5; 31,0] (p=0,009). At the end of inpatient treatment, patients underwent echocardiography. Death and myocardial infarction were monitored during hospitalization and for 12 months after discharge.Results. During hospitalization, 2 patients died (4,7%; one in each group, p=1,00). No recurrent MI were reported. The left ventricular ejection fraction in the PCI group was 50 [46; 54] %, in the group with drug therapy — 43 [38; 50] % (p=0,01). Out of 43 included patients, long-term outcomes were followed up in 32 (74%). Among them, 1 (5,8%) patient died in group 1, 6 (33,3%) patients — in group 2 (p=0,04). In total, death or recurrent MI in the first group was observed in 2 (12%) patients, in the second group — in 5 (33%) patients (p=0,14).Conclusion. Revascularization of a fully occluded culprit coronary artery in stable patients with STEMI after 48 hours of symptoms’ onset is associated with a higher inhospital left ventricular ejection fraction and a decrease in 12-month mortality.

Wasp sting induced STEMI with complete coronary artery occlusion: a case of Kounis syndrome

A 45-year-old previously healthy man with minimal coronary artery disease on imaging presented with an acute MI after sustaining a wasp sting following previous non-eventful exposures throughout his life. This...

Myocardial Infarction Related to Trauma.

Myocardial infarction (MI) secondary to acute coronary occlusion related to trauma is rare. A previously healthy man developed acute MI shortly after a motor vehicle accident. This case illustrates the feasibility of primary percutaneous coronary intervention for acute MI due to complete coronary artery occlusion related to trauma, including the use of manual thrombectomy, stents, and dual antiplatelet therapy. This approach requires the intervention of a multidisciplinary team in a Level 1 trauma center that can rapidly evaluate the patient and rule out other life-threatening injuries that could preclude antiplatelet therapy.

Abstract 18134: Cardiomyocyte Overexpression of the alpha1A-Adrenergic Receptor in the Rat Protects Post-Infarct Heart Failure through Angiogenesis and the MEK-ERK Pathway

α1A-Adrenergic receptors (α1A-AR) are important for regulating cardiac contractility, but whether they regulate coronary vessels is not known. To examine this we investigated the effects of chronic, complete coronary artery occlusion (CAO) in rats with cardiac myocyte-restricted transgenic (TG) α1A-AR overexpression, since protection of the heart with complete CAO requires increased blood flow. 4 weeks after permanent left anterior descending CAO TG rats displayed improved contractility vs. non-transgenic littermates (NTL) (n=8/group, p&lt;0.05): 23% higher in LV dP/dt (7188±167mmHg/s), 13% higher in LV ejection fraction (57±0.9) and 23% lower in end-systolic wall stress (LVSWS) (79±6dynes/cm2) compared to NTLs. The scar size at 4 wks after CAO was significantly smaller in TG rats (18±2%) compared to NTL rats (28±3%), p&lt;0.05, but more importantly there were increased blood vessels within the scar in the TG rat hearts suggesting angiogenesis. This was confirmed using colored microspheres to measure coronary blood flow, which was higher in area at risk in TGs (1.4±0.2ml/min/g) as compared to NTLs (0.5±0.08ml/min/g), p&lt;0.05. This increased blood flow was further supported by a 41% increase in arterial density within the ischemic zone compared to NTLs at 2 weeks after CAO. In addition, capillary density was also found to be significantly increased, by 18% in the remote zone, compared to 2109 caps/mm2 in NTL. Utilizing an In vitro model, treatment with 25μM A61603 for 48 hours in cultured NTL neonatal myocytes resulted in an increase in VEGF-A secretion into the culture media and 26% increase in vascular tubule formation in HUVECs by a paracrine mechanism coinciding with an increased VEGF-A concentration compared to vehicle treated myocytes. Since VEGF is linked to the MEK-ERK signaling pathway, we blocked this mechanism by chronically administering the MEK blocker, U0126, sc. In these rats LV function was no longer different after 4 wks permanent CAO in TG and WTL treated with the blocker. Therefore, overexpression of cardiac myocyte specific α1A-AR in rats protected against cardiac dysfunction and remodeling associated with chronic myocardial infarction through the MEK-ERK pathway and via angiogenesis with a VEGF-A related paracrine mechanism.

Pulsatile biventricular assist device and an absent mitral valve

CONCLUSIONS In cases of acute aortic dissection, the potential for a circumferential intimal tear needs to be considered because intimo-intimal intussusception, although rare, is a serious complication of aortic dissection. Coronary angiography may indicate complete coronary artery occlusion that may be due to the intussuscepting flap and will resolve once the aortic defect has been repaired. Intraoperative

Qualitative and Quantitative Coronary Angiography in patients with Acute Coronary Syndrome (ACS)

Background and AimAcute Coronary Syndrome (ACS) encompasses several diseases, previously thought to be separate and defined disease states. In this syndrome, Unstable Angina (UA), Non-ST Elevation Myocardial Infarction (NSTEMI), and ST-Elevation Myocardial Infarctions (STEMI) are all part of this category. The pathogenesis begins with plaque rupture which activates the platelets and coagulation cascade leading to thrombus formation. The thrombus leads to partial or complete coronary artery occlusion leading to various clinical manifestations of ACS.The aim of the present study is to assess the extent of coronary artery disease and characterizes plaque morphology and lesion severity in patients with ACS in comparison with patients with chronic stable ischemic heart disease. Subjects and MethodsTo achieve this aim, we studied 100 patients with symptomatic coronary artery disease admitted to Mansoura medical Hospital, where they were subjected to full clinical evaluation; 12 lead electrocardiogram, full laboratory investigations and Coronary angiography was done to every patient, then we analyses the results both qualitative (eye ball description of angiographic lesions) and quantitative (computer-based). Those patients were classified into two main groups, the first group of patients were those with ACS (50 patients) as a test group while the second one included patients chronic stable ischemic heart disease (50 patients) as a control group. ResultsBoth groups were comparable and no significant difference was present as regard age, sex, diabetes mellitus, hypertension, smoking, left ventricular function, prior PTCA, prior CHF and angina class while, prior MI more frequent among test group. One hundred, forty-seven lesions (66 in test group and 81 in control group) were available for detailed qualitative angiographic analysis. Out of seven criteria analyzed only presence of lumen irregularity and thrombus were more frequent among patient who presented with ACS (17 (26%) vs. 2 (2.5%) p<0.05; 9 (13.6%) vs. 0 (0%) p<0.05) respectively), and this represents the main finding in the current study. No significant difference was present in Quantitative Coronary angiographic characteristics in both groups. ConclusionThe qualitative angiographic assessment represents an essential tool in the evaluation and risk stratification of patients with ACS, through the demonstration of the presence of thrombus and lumen irregularity that correlated more with ACS than the other studded criteria. In addition, QCA although added accurate assessment of the degree of luminal narrowing, thus helping in assessment of the severity of the disease.

Comparison of Hemorheological Variables in ST-Elevation Myocardial Infarction Versus Those in Non-ST-Elevation Myocardial Infarction or Unstable Angina Pectoris

The aim of this study was to evaluate hemorheologic variables in patients with acute coronary syndromes in relation to the occurrence of ST-segment elevation myocardial infarction (STEMI). In 370 consecutive patients with acute coronary syndromes, 215 with STEMIs and 155 with non-ST-segment elevation myocardial infarctions or unstable angina pectoris, who underwent percutaneous coronary intervention, hemorheologic studies were performed by assessing whole-blood viscosity (at shear rates of 0.512 and 94.5 s(-1)), plasma viscosity, and erythrocyte deformability index. A significant difference in hematocrit and in whole-blood viscosity at 0.512 s(-1) was found between the 2 groups of patients. Hematocrit at admission in the highest tertile compared with the lowest tertile remained independently associated with the occurrence of STEMI on multivariate analysis adjusted for traditional cardiovascular risk factors, previous coronary artery disease, multivessel disease, bleeding complications, and leukocyte count. In conclusion, erythrocyte concentration seems to play a role per se in the occurrence of STEMI and complete coronary artery occlusion and might be considered in stratifying high-risk cardiovascular patients and as a possible therapeutic target in patients presenting with acute coronary syndromes.

Intravenous streptokinase infusions in acute myocardial infarction. Restoring patency of occluded thrombotic coronary vessels (author's transl)

Intravenous treatment over 30 minutes with 500 000 U streptokinase was given to 21 patients with acute myocardial infarction. Serial measurements of serum CK-MB activity made recanalisation of the infarcted artery likely in 3 patients. Selective coronarography was performed in 18 patients during the acute infarction phase. Angiographic follow-up investigations were done 24 hours and after 3 weeks. In 3 cases only subtotal occlusion of the infarcted coronary artery was seen during the acute phase. A thrombus demonstrated in two patients could be lysed. In 8 out of 15 patients with complete coronary artery occlusion the infarcted vessel was reopened 20-60 minutes after onset of intravenous streptokinase infusion. In a further 4 patients recanalisation was observed 60-140 minutes after passing a guide wire or during an additional intracoronary infusion of streptokinase. The infarcted vessel remained occluded in 3 patients, one of whom died following myocardial rupture. In 12 patients with recanalisation of the infarcted artery during the acute phase a premature maximum of serial CK-MB serum activity was seen after 13.5 +/- 2.9 hours in comparison with 20.9 +/- 5.3 hours in 122 patients treated conventionally. Serial enzyme determinations allow indirect conclusions as to a rapid recanalisation of an infarcted blood vessel.

Bidirectional Role of Tumor Necrosis Factor-α in Coronary Microembolization

In patients with unstable angina, plaque rupture and coronary microembolization (ME) can precede complete coronary artery occlusion and impending infarction. ME-induced microinfarcts initiate an inflammatory reaction with increased tumor necrosis factor-alpha (TNF-alpha) expression, resulting in progressive contractile dysfunction. However, TNF-alpha is not only a negative inotrope but can also protect the myocardium against infarction. In anesthetized pigs, we studied whether ME protects against infarction when TNF-alpha expression is increased. ME (group1; n=7) was induced by intracoronary infusion of microspheres (42 microm; 3000 per mL/min inflow). Controls (group 2; n=8) received saline. Groups 3 and 4 (n=4 each) were pretreated with ovine TNF-alpha antibodies (25 mg/kg body weight) 30 minutes before ME or placebo, respectively. Ischemia (90 minutes) was induced 6 hours after ME when TNF-alpha was increased (66+/-21 pg/g wet weight; mean+/-SEM) or after placebo (TNF-alpha, 21+/-10 pg/g; P<0.05). Infarct size (percentage area at risk) was determined after 2 hours of reperfusion (triphenyl tetrazolium chloride staining). ME decreased systolic wall thickening progressively over 6 hours (group 1 versus group 2, 65+/-4% versus 90+/-1%; percentage of baseline; P<0.05). TNF-alpha antibodies attenuated the progressive decrease in systolic wall thickening following ME (group 3, 77+/-5% of baseline; P<0.05 versus group 1) with no effect in controls (group 4; 90+/-8% of baseline). With ME, infarct size was decreased to 18+/-4% versus 33+/-4% in group 2 (P<0.05). The infarct size reduction was abolished by TNF-alpha antibodies (group 3 versus group 4, 29+/-3% versus 35+/-5%). In ME, TNF-alpha is responsible for both progressive contractile dysfunction and delayed protection against infarction.

Assessment by radionuclide ventriculography of postischemic regional left ventricular dysfunction in patients with healed myocardial infarction or angina pectoris

Postischemic left ventricular (LV) dysfunction has been observed in experimental animal models after brief, complete coronary artery occlusion followed by reperfusion, but less relevant information is available for humans. The incidence and duration of postischemic LV dysfunction was examined by exercise radionuclide ventriculography in 50 patients with coronary artery disease. Cardiac imaging was performed at rest and was repeated during exercise and then immediately after and 5, 10, and 20 minutes after exercise. LV regional wall motion abnormalities were noted in 50 segments during exercise; they persisted in 30 of 50 segments after exercise, and remained apparent for 20 minutes in 11 segments. In contrast, in 33 segments, wall motion abnormalities were noted only after exercise and continued for 20 minutes in 13 of 33 segments. Exercise-related wall motion abnormalities were observed in 63 segments (76%) after exercise, and in 24 of 63 segments abnormalities continued for 20 minutes after exercise, although parameters of LV hemodynamic functions approached normal values after exercise. The mechanism of postexercise dysfunction is considered to involve acute myocardial stunning after a brief episode of myocardial ischemia, whereas regional wall motion abnormalities observed only after exercise seem to be related to increased levels of catecholamines or sympathetic overdrive, which mask less significant myocardial ischemia during exercise.

Post-endsystolic active shortening in the non-ischemic region impairs left ventricular pressure fall in acute ischemic heart.

To investigate the relation between the impairment of isovolumic relaxation and the regional wall motion in acute ischemia, the left ventricular pressure fall and regional myocardial motion were examined in the relaxation phase in dogs during both acute coronary artery occlusion (n = 12) and a regional coronary flow reduction (n = 6). Fifteen to 40 seconds after complete coronary artery occlusion or in the stable state after a regional coronary flow reduction by 70 to 90% of the control state, a shortening of the non-ischemic region at the early isovolumic relaxation phase (the post-endsystolic shortening) appeared, combined with lengthening of the ischemic region. In these situations, the logarithmic plots of the left ventricular pressure fall was composed of two components (time constant of early part [Ta] and at latter part [Tb]). Ta was greater than Tb (64.3 +/- 13.8 milliseconds vs. 36.6 +/- 10.4 milliseconds at 15 seconds after coronary occlusion, p < 0.01; 67.6 +/- 22.9 milliseconds vs. 45.1 +/- 17.5 milliseconds at flow reduction, p < 0.01) and the time constant at control (p < 0.01). These findings suggested that post-endsystolic shortening in the non-ischemic region played a role in a the non-uniformity of the left ventricular contraction and contributed to the impairment of the left ventricular pressure fall in acute regional ischemia, especially in early isovolumic relaxation.

Therapy of unstable angina with the low molecular weight heparins

Unstable angina is in most cases caused by partial or complete coronary artery occlusion due to the disruption of an atherosclerotic plaque and to thrombus formation. An immediate antithrombotic approach is essential to prevent fatal and non-fatal myocardial infarction, and the combination of aspirin and unfractionated heparin has played a pivotal role in the past years. Low molecular weight heparins have improved pharmacokinetic and pharmacodynamic properties over unfractionated heparin that have resulted in greater efficacy and safety in the field of venous thromboembolism. Low molecular weight heparins can be administered by once or twice daily subcutaneous injections at fixed, weight-adjusted doses without the need for monitoring. Because of their potential, many recent clinical trials have evaluated their efficacy and safety in the management of patients with unstable angina. Three low molecular weight heparins have so far been tested: nadroparin, dalteparin and enoxaparin. The results of the published trials confirm that the newer compounds are at least as safe and effective as unfractionated heparin, and offer considerable therapeutic advantages. Nevertheless, the different properties of the three compounds and perhaps the different designs of the clinical trials have led to not entirely comparable findings.