Cause Of Myocardial Ischemia Research Articles

Microvascular coronary dysfunction affects global longitudinal strain after stress echocardiography

Abstract Funding Acknowledgements Type of funding sources: None. BACKGROUND. Coronary microvascular dysfunction (CMD) is a potential cause of myocardial ischemia and may affect myocardial function at rest and during stress. CMD can be identified, in patients with non-obstructive coronary artery disease (CAD), by a reduced transthoracic Doppler-derived coronary flow reserve (CFR), which is an index of coronary arterial reactivity, and can be impaired in both obstructive CAD and CMD. The aim of this study was to investigate the dipyridamole-induced changes of left ventricular (LV) global longitudinal strain (GLS) in patients with CMD. METHODS. 59 patients (39% women, mean age 65.6 ± 6.1 years) with history of chest pain and without obstructive coronary artery disease (CAD) underwent dipyridamole stress echocardiography. Coronary flow was assessed in the left anterior descending coronary artery. Coronary flow reserve (CFR) was determined as the ratio of hyperaemic to baseline diastolic coronary flow velocity. CMD was defined as CFR < 2. GLS was measured at rest and at peak dose, using automated function imaging, through the positioning of three endocardial markers (two markers at the mitral annulus and one at the apex) in each apical view. Subsequently, the obtained segmental values of GLS were visualized as a bull’s-eye map in a quick and feasible manner. We had optimal left ventricular endocardial tracking in the overall population. In each patient, we used a frame rate of 70 frames/sec for adequate 2D strain analysis. We analyzed GLS at each step of stress test and compared peak-dose values with baseline. RESULTS. Nineteen patients (32%) among the overall population showed CMD. Baseline GLS was significantly lower in patients with CMD (-16.8 ± 2.7 vs. -19.1 ± 3.1, p < 0.01). A different contractile response to dipyridamole infusion was observed between the two groups: GLS significantly increased up to peak dose in patients without CMD (from -19.1 ± 3.1 to -20.2 ± 3.1, p < 0.01), and significantly decreased in patients with CMD (from -16.8 ± 2.7 to -15.8 ± 2.7, p < 0.01). There was a significant inverse correlation between CFR and DGLS (r = -0.82, p < 0.01). CONCLUSIONS. GLS analysis, particularly performed by comparing dipyridamole peak-dose with baseline values, shows that in patients with CMD there is a different response of LV myocardium to stress test. It could be assumed that the inverse correlation between CFR and delta GLS reflects a progressive subclinical worsening of LV myocardial function and lack of LV contractile reserve due to underlying myocardial ischemia. Larger studies could confirm our data. Abstract Figure. Abstract Figure.

Surgical treatment of obstructive hypertrophic cardiomyopathy combined with muscle bridging of the left anterior descending artery

Myocardial bridging is often detected during diagnostic coronary angiography in patients with congenital and acquired heart defects. In most cases, muscle bridging does not require surgical treatment. Myocardial bridging and tunnels causing compression of one or more major coronary arteries is a potential cause of myocardial ischemia in patients with hypertrophic cardiomyopathy. The authors report surgical treatment of a patient with obstructive hypertrophic cardiomyopathy and myocardial bridging of the left anterior descending artery.

A study of arginase-1 activity and lipid profile in patients with myocardial infarction

Myocardial necrosis caused by ischemia is called a myocardial infarction (MI). which interrupts coronary blood supply. When the oxygen supply to the heart is insufficient to meet metabolic demands, myocardial ischemia occurs. Atherosclerosis, which obstructs the coronary arteries, is the most common underlying cause of myocardial ischemia. The role of arginase-1 (ARG-1) and serum lipids in the pathogenesis of myocardial infarction is becoming clearer. This study aims to see if there is a link between ARG-1 activity and MI in the Iraqi population. Between the first of November 2021 and the first of February 2022, 90 people were separated into two groups: 45 patients with MI and 45 healthy controls. Human ARG-1 was measured in serum blood using the ELISA method. The serum lipid was measured using the spectrophotometry technique. The current investigation discovered a substantial (p=0.01) rise in ARG-1 concentration compared to control groups, as well as a significant difference in blood lipid content between patients and control groups (p<0.05). Finally, ARG-1 may have a role to play role in the pathogenesis of MI.

236 Variation in cardiac troponin I serum levels after ECG exercise stress test in patients with microvascular angina

Abstract Aims Cardiac troponin I (cTnI) is considered a marker of myocardial necrosis. However, several studies have shown that cTnI increases also after short episodes of myocardial ischaemia. Nevertheless, it is unknown whether the changes in cTnI show differences according to the cause of myocardial ischaemia. Thus, our study aimed to evaluate cTnI response to ischaemia in patients with stable coronary artery disease (CAD), patients with microvascular angina (MVA), and transient ischaemia induced during percutaneous coronary intervention (PCI). Methods and results We studied four groups of patients: (1) patients with stable angina and obstructive CAD (coronary stenosis ≥50% and/or fractional flow reserve <0.80) (Group 1, n = 8); (2) patients with stable angina but no obstructive CAD and a final diagnosis of MVA according to positive intracoronary acetylcholine provocation test and/or coronary flow velocity reserve assessment with transthoracic Doppler echocardiography (Group 2, n = 20); (3) patients with stable angina and obstructive CAD undergoing PCI (Group 3, n = 10); (4) a control group of healthy subjects, with no history of cardiovascular disease (CVD) (Group 4, n = 20). Patients in groups 1, 2, and 4 underwent ECG exercise stress test (EST) according to a standard treadmill Bruce protocol. Peripheral venous blood samples were collected immediately before, at the end and 1, 3, and 24 h after test ending. Patients in group 3 underwent PCI with at least one drug-eluting stent implantation. Peripheral venous blood samples were collected immediately before, at the end and 1, 3, and 24 h after PCI ending. High-sensitivity cTnI (hs-cTnI) levels were measured by chemiluminescent microparticle immunoassay (CMIA). The main results of hs-cTnI in the four groups of patients are summarized in the table. Basal hs-cTnI serum levels were significantly higher in group 3, while there were no significant differences among groups 1, 2, and 4. Hs-cTnI serum levels significantly increased in all groups in response to the procedure (EST or PCI). A greater increase of hs-cTnI was found in group 3 (peak level at 24 h) compared to the other groups (peak level at 3 h). Furthermore, among patients undergoing EST, a significantly higher hs-cTnI increase was found in healthy subjects, compared to patients with CAD and MVA. Heart rate (HR) during stress test (both as an absolute value and predicted maximal HR for age) was the only variable statistically predictive of hs-cTnI increase during EST (HRmax: r 0.289, P 0.04; %HRmax: r 0.307; P 0.03). On the other hand, no clinical and laboratory variable was associated to hs-cTnI response after PCI. Conclusions Hs-cTnI serum levels increase after EST, both in patients with obstructive CAD and coronary microvascular dysfunction (CMD), but a similar increase is also observed in healthy subjects. More consistent hs-cTnI level increase with later peak-level is observed in patients with obstructive CAD after transient ischaemia induced during PCI.

Early Presentation of Patients with Abnormal Origin of Left Coronary Artery from the Pulmonary Artery is a Predictor of Poor Mid-term Outcomes.

Abnormal origin of left coronary artery from the pulmonary artery (ALCAPA) is one of the most common causes of myocardial ischemia and infarction in childhood. This study aimed to determine the correlation between age at clinical presentation, level of ventricular dysfunction, and post-repair outcomes. This is retrospective study from 1993 to 2018 including thirty-one patients. The study cohort was divided into two groups according to age (< 6 months, > 6 months). The significance level was set at p 0.05.The median follow-up time was 72 [24–168] months. Median age was 4.7 [2.3–16] months. Median weight was 6.2 [4.3–9] kg. There was severe left ventricular (LV) dysfunction (ejection fraction < 35%) in 64.5% of patients. Mitral regurgitation (MR) was moderate to severe in 13 patients (41.9%). Two patients (6.4%) required extracorporeal membrane oxygenation (ECMO) support before surgery and 6 (19.4%) after correction. Age < 6 months was significantly associated with severe clinical presentation, severe LV dysfunction, delayed sternal closure, prolonged respiratory mechanical support, and prolonged length of ICU stay (p = 0.024, p = 0.042, p = 0.002, p = 0.042, p = 0.022, respectively). After surgery, ejection fraction improved to a median of 57% [50.7–60.5]. MR regressed in 12 patients (92.3%). Mortality rate after surgery was 9.7%. All patients were free from reoperation at the last follow-up. Young age at diagnosis was significantly associated with a more severe clinical presentation and poorer outcomes. After re-establishment of a two-coronary circulation, both ventricular function and MR tend to normalize over time regardless of age at repair.

Abstract 9524: The Challenge of Treating a Previously Surgical Revascularized Patient With Acute ST-Elevation Myocardial Infarction (STEMI) and Coronary-Subclavian Steal Syndrome

Introduction: Coronary-subclavian steal syndrome (CSSS) is a rare cause of myocardial ischemia after coronary artery bypass grafting (CABG), due to significant stenosis of the proximal portion of the left subclavian artery. It is characterized by blood flow inversion in the left internal thoracic artery, diverting the blood flow from the coronary artery to the left medio-distal subclavian artery. We report a case of a patient who underwent complex surgery to correct the CSSS. Case report: A 70-year-old male patient, with history of both percutaneous coronary intervention (PCI) of the right coronary artery and CABG, was admitted to the emergency room with STEMI and complete atrioventricular block. He was initially managed to the cath lab where a transvenous pacemaker was implanted and coronary angiography showed occlusion of the left main, proximal right coronary and left subclavian arteries. Only saphenous vein - second marginal graft was patent and, despite severe stenosis in the proximal portion of the circumflex artery, this artery was responsible for irrigation of the entire left coronary system, as well as retrograde filling of the left internal thoracic artery - anterior descending artery graft. A conservative approach was proposed. For a better anatomically interpretation, coronary angiotomography was indicated and showed obstruction of the left subclavian artery after its origin, with 2.2cm length and refilling before the origin of the ipsilateral vertebral and internal mammary arteries. In addition, most visceral branches demonstrated severe atherosclerosis, and the right common iliac artery and left external iliac artery were occluded. After discussion with the Heart Team, it was decided to perform a left carotid-subclavian graft with a segment of the saphenous vein. The procedure was successful, with no complications and lasted 5 hours. The patient was discharged from hospital one week later. Discussion: CSSS is rare and difficult to treat. The most common treatment is angioplasty of the subclavian artery, which was not possible in this case due to the lack of femoral access and the extension of the occlusion. In this patient, with a high risk of death, the bypass surgical revascularization with saphenous graft became the only feasible treatment.

HIF in the heart: development, metabolism, ischemia, and atherosclerosis.

The heart forms early in development and delivers oxygenated blood to the rest of the embryo. After birth, the heart requires kilograms of ATP each day to support contractility for the circulation. Cardiac metabolism is omnivorous, utilizing multiple substrates and metabolic pathways to produce this energy. Cardiac development, metabolic tuning, and the response to ischemia are all regulated in part by the hypoxia-inducible factors (HIFs), central components of essential signaling pathways that respond to hypoxia. Here we review the actions of HIF1, HIF2, and HIF3 in the heart, from their roles in development and metabolism to their activity in regeneration and preconditioning strategies. We also discuss recent work on the role of HIFs in atherosclerosis, the precipitating cause of myocardial ischemia and the leading cause of death in the developed world.

Interplay Between Myocardial Bridging and Coronary Spasm in Patients With Myocardial Ischemia and Non-Obstructive Coronary Arteries: Pathogenic and Prognostic Implications.

BackgroundMyocardial bridging (MB) may represent a cause of myocardial ischemia in patients with non‐obstructive coronary artery disease (NOCAD). Herein, we assessed the interplay between MB and coronary vasomotor disorders, also evaluating their prognostic relevance in patients with myocardial infarction and non‐obstructive coronary arteries (MINOCA) or stable NOCAD.Methods and ResultsWe prospectively enrolled patients with NOCAD undergoing intracoronary acetylcholine provocative test. The incidence of major adverse cardiac events, defined as the composite of cardiac death, non‐fatal myocardial infarction, and rehospitalization for unstable angina, was assessed at follow‐up. We also assessed angina status using Seattle Angina Questionnaires summary score. We enrolled 310 patients (mean age, 60.6±11.9; 136 [43.9%] men; 169 [54.5%] stable NOCAD and 141 [45.5%] MINOCA). MB was found in 53 (17.1%) patients. MB and a positive acetylcholine test coexisted more frequently in patients with MINOCA versus stable NOCAD. MB was an independent predictor of positive acetylcholine test and MINOCA. At follow‐up (median, 22 months; interquartile range, 13–32), patients with MB had a higher rate of major adverse cardiac events, mainly driven by a higher rate of hospitalization attributable to angina, and a lower Seattle Angina Questionnaires summary score (all P<0.001) compared with patients without MB. In particular, the group of patients with MB and a positive acetylcholine test had the worst prognosis.ConclusionsAmong patients with NOCAD, coronary spasm associated with MB may predict a worse clinical presentation with MINOCA and a higher rate of hospitalization attributable to angina at long‐term follow‐up with a low rate of hard events.

The Beneficial influence of Rosemary Aqueous Extract on the treatment of oxidative stress-induced myocardial Ischemia in Rats. Z. H. AL-Qaisi1, S. M. Abbood1, M. T. Mohammed *1, S. M. Kadhim2 1Department of Chemistry, College of Science, Mustansiriya University, Iraq 2Ministry of Education, Rusafa-1, Iraq *Corresponding author: dr.mustafa@uomustansiriyah.edu.iq

Abstract Ischemia “stroke” may occur in various combinations of clinical illnesses. The effects of such an Ischemic represent a serious problem. Oxidative stress has been shown to act as one of the main causes of Myocardial Ischemia- Reperfusion Injury (IR). Reperfusion injury is defined as the action of returning the flow of blood to an organ or tissue after a period of stroke or myocardial infarction (MI). R. Officinalis (Rosemary) has a diverse therapeutic against many illnesses. Further, recent evidence also gives R. Officinalis a major role in protecting diverse organs from harmful oxidative stress. So, R.Officinalis seems like a good protect to the myocardial against the IR Injury. The study included the components of essential oils of the rosemary leaves in the watery extract and determine whether rosemary protects form Ischemia-Reperfusion induced myocardial ischemia. We divided forty-five Wister rats into three groups Group 1 as the control group, Group 2 underwent surgery without extract therapy, and Group 3 with extract therapy. Wister rats in Group 2, and Group 3 underwent myocardial ischemia for 45 min followed by 90 min period of Reperfusion. Animals in group 3 received rosemary (1 mL/g) for 14 days also, before Ischemia, and before Reperfusion. We found that the extract comprises from many essential oils. The levels of cardiac markers (AST, ALT, and LDH) and Oxidative stress markers (NO, and LPO) in group 3 a significantly decreased compared to group 2. Based on the results, the R.Officinalis treatment lessens the effect of Ischemia-Reperfusion on the rat’s heart, including the induce myocardial infarction.

Appropriate ICD Interventions for Ventricular Arrhythmias Are Predicted by Higher Syntax Scores I and II in Patients with Ischemic Heart Disease.

Aims. The occurrence of ventricular arrhythmias (VAs) in ischemic heart disease (IHD) patients is related to the presence and extent of fibrotic/scar tissue. As coronary atherosclerosis is the underlying cause of myocardial ischemia and fibrosis, in IHD patients implanted with an implantable cardioverter defibrillator (ICD) we investigated the relation between the VA burden and the complexity of coronary atherosclerotic lesions. Methods and results. In IHD patients who underwent coronary angiography and ICD implant, the Syntax scores I and II (SSI-II), as index of the severity of the coronary atherosclerotic disease, and the occurrence of VA were assessed. Overall 144 patients were included (123 males). Of these 22 patients (15%) experienced at least one episode of VA (cycle length 298 ± 19 msec) that required ICD intervention. The number of episodes per patient and per year was 4 ± 6 and 2.8 ± 4, respectively. Patients that experienced a VA compared to those free from arrhythmic events did not have distinct baseline clinical characteristics except for a higher SS I and SS II (21 (IQR 13–38) vs. 16 (IQR 10–23); p = 0.037; and 50 (IQR 39–62) vs. 42 (IQR 34–50); p = 0.012). In the binary logistic regression analyses the SS I and II were the only independent predictors of VA occurrence. A higher SS II was also associated with an earlier time to first event (p = 0.005). Conclusion. Higher SS I-II scores reflect a more severe coronary atherosclerosis and are associated with a greater VA burden. Further studies are needed to better clarify the ability of SSI-II to stratify the risk of IHD patients to develop life-threatening VA.

ALCAPA syndrome: A rare etiology of cardiac arrest in a teenager.

ALCAPA syndrome is a rare congenital heart disease and a cause of myocardial ischemia in pediatric population. The authors present the case of a 10-year-old girl admitted to the emergency room after experiencing cardiac arrest at school. In the echocardiogram, the inability to identify the origin of the left coronary artery raised the hypothesis of abnormal origin of the left coronary artery from the pulmonary artery (ALCAPA). A CT-scan and a cardiac catheterization were performed confirming the diagnosis. Infants with the syndrome may have myocardial infarction and congestive heart failure. She successfully underwent cardiac surgery. Most undiagnosed patients die within the first year of life, and it is necessary to develop an extensive network of collaterals to ensure survival. ALCAPA syndrome rarely manifests in late childhood, teenagers, and adults and may be an important cause of sudden cardiac arrest.

Microvascular Angina, on the Purpose of a Case from Southern Colombian

The most common cause of myocardial ischemia and angina is coronary stenosis by atheromatous lesions in the epicardial arteries. However, a significant percentage of patients with angina and ischemia demonstrated by tests to induce it not present coronary obstructions on angiography. For this reason, the case of a 68-year-old woman is presented, who consulted for chest pain with typical oppressive characteristics, associated with autonomous symptoms, with electrocardiographic changes and elevated cardiac enzymes, given the above she received anti-ischemic, antiplatelet, and analgesic, which required coronary stratification, which was later reported within normal limits. Likewise, outpatient follow-up was carried out 3 months after the cardiovascular event, reporting within normal limits. In these cases, it is attributed to coronary spasm, endothelial dysfunction, and myocardial metabolism disorders as responsible for ischemia and its clinical manifestations. This situation constitutes a frequent and costly clinical problem, contributes to diminishing the quality of life, and presents a challenge in the diagnosis and treatment. This form of angina is not as benign as it was previously considered. We present a case in which it was not possible to demonstrated ischemia by tests performed and coronary angiography revealed no obstructive lesions.

Abstract 12727: Microvascular Coronary Dysfunction Affects Global Longitudinal Strain After Dipyridamole Stress Echocardiography

Introduction: Coronary microvascular dysfunction (CMD) is a potential cause of myocardial ischemia and may affect myocardial function. CMD can be identified, in patients with non-obstructive coronary artery disease (CAD), by a reduced transthoracic Doppler-derived coronary flow reserve (CFR), which is an index of coronary arterial reactivity. Hypothesis: The aim of this study was to investigate the dipyridamole-induced changes of global longitudinal strain (GLS) in patients with CMD. Methods: fiftythree patients (35M, 18F; mean age 67±8 years) without obstructive CAD, assessed by invasive coronary angiogram, underwent dipyridamole stress echocardiography. CFR were determined as the ratio of hyperaemic to baseline diastolic coronary flow velocity. CMD was defined as CFR &lt; 2. GLS was visualized as a bull’s-eye map in a quick and feasible manner. In each patient, we used a frame rate of 70 frames/sec for adequate 2D strain analysis. We analyzed GLS at each step of stress test and compared peak-dose values with baseline. Results: Sixteen patients (30%) among the overall population showed CMD. There were no significant differences in baseline characteristics between patients with or without CMD. GLS, at baseline, was significantly lower in patients with CMD (-16.7±3.77 vs. -17.9±3.75 - p&lt;0.01). We observed a different response to dipyridamole stress echocardiography, between the two groups: GLS significantly increased up to peak dose in patients without CMD (from -17.9±3.75 to -19.5±4.12 - p&lt;0.01), whereas on the other hand, a significant decrease from rest to peak dose was observed in patients with CMD (from -16.7±3.77 to -15.4±4.21- p&lt;0.01). There was a significant inverse correlation between CFR and delta GLS measured at rest and after dipyridamole peak dose (r = -0.83 - p&lt;0.01). Conclusions: GLS analysis, performed by comparing dipyridamole peak-dose with baseline values, shows that in patients with CMD there is a different response of left ventricular myocardiim to stress test. It could be assumed that the inverse correlation between CFR and delta GLS reflects a progressive subclinical worsening of left ventricular myocardial function in these patients. Larger studies could confirm our data.

Inverse response of global longitudinal strain after dipyridamole stress echocardiography in patients with microvascular coronary dysfunction

Abstract Background Coronary microvascular dysfunction (CMD) is a potential cause of myocardial ischemia and may affect myocardial function at rest and during stress. CMD can be identified, in patients with non-obstructive coronary artery disease (CAD), by a reduced transthoracic Doppler-derived coronary flow reserve (CFR), which is an index of coronary arterial reactivity, and can be impaired in both obstructive CAD and CMD. The aim of this study was to investigate the dipyridamole-induced changes of global longitudinal strain (GLS) in patients with CMD. Methods 43 patients (29M, 14F; mean age 68±7 years) without obstructive CAD, assessed by invasive coronary angiogram, underwent dipyridamole stress echocardiography. Coronary flow was assessed in the left anterior descending coronary artery (LAD) and was identified as the colour signal directed from the base to the apex of the left ventricle, containing the characteristic biphasic pulsed-Doppler flow signals. CFR were determined as the ratio of hyperaemic to baseline diastolic coronary flow velocity. CMD was defined as CFR &amp;lt;2. GLS was measured using automated function imaging, through the positioning of three endocardial markers (two markers at the mitral annulus and one at the apex) in each apical view. Subsequently, the obtained segmental values of GLS were visualized as a bull's-eye map in a quick and feasible manner. We had optimal left ventricular endocardial tracking in the overall population. In each patient, we used a frame rate of 70 frames/sec for adequate 2D strain analysis. We analyzed GLS at each step of stress test and compared peak-dose values with baseline. Results Thirteen patients (30%) among the overall population showed CMD. There were no significant differences in baseline characteristics between patients with or without CMD. GLS, at baseline, was significantly lower in patients with CMD (−16.9±3.78 vs. −17.8±3.77 – p&amp;lt;0.01). We observed a different response to dipyridamole stress echocardiography, between the two groups: GLS significantly increased up to peak dose in patients without CMD (from −17.8±3.77 to −19.3±4.09 – p&amp;lt;0.01), whereas on the other hand, a significant decrease from rest to peak dose was observed in patients with CMD (from −16.9±3.78 to −15.5±4.18 – p&amp;lt;0.01). There was a significant inverse correlation between CFR and delta GLS measured at rest and after dipyridamole peak dose (r=−0.82 – p&amp;lt;0.01). Conclusions GLS analysis, particularly performed by comparing dipyridamole peak-dose with baseline values, shows that in patients with CMD there is a different response of left ventricular myocardiim to stress test. It could be assumed that the inverse correlation between CFR and delta GLS reflects a progressive subclinical worsening of left ventricular myocardial function in these patients. Larger studies could confirm our data. Funding Acknowledgement Type of funding source: None

Risk Factors in Patients with Non-ST Segment Elevation Myocardial Infarction.

Introduction:The most common cause of myocardial ischemia is atherosclerotic epicardial coronary artery disease, present in 90% of patients. Risk factors positively correlate with the onset, development and subsequent complications of atherosclerotic disease.Aim:Determine the percentage frequency of classic risk factors for coronary disease in patients with non-ST segment elevation myocardial infarction (NSTEMI), with regard to gender.Methods:A retrospective study was conducted on 600 respondents, treated for NSTEMI at the Clinic for Internal Medicine of the University Clinical Center (UKC) Tuzla, in the period from June 2016 to December 2019.Results:Overall, smoking was the leading risk factor (65%), followed by hypertension (58%), hyperlipoproteinemia (39%), overweight (33%), positive family burden (30%) and diabetes mellitus (19%). In male patients, the leading risk factor was smoking, rating at 74%, while in female patients – it was hypertension at 67%. In younger groups of patients leading risk factors were smoking and a positive family burden.Conclusion:With adequate prevention and treatment measures, a significant reduction in the prevalence of the cardiovascular disease can be achieved, since the risk factors for its development have long been known. Quitting smoking is one of the most effective secondary prevention measure since it reduces the reinfarction risk rate by 50%. Knowledge of coronary risks, as well as success in reducing them, can greatly contribute to patients’ overall sense of contentment and significantly raise their self-confidence.

Referral Bias in Coronary Micro vascular Dysfunction: a Retrospective Study

Obstructive coronary artery disease (CAD) is a well-defned condition and a signifcant cause of myocardial ischemia. Patients with angina typically undergo non-invasive cardiac investigations initially as a means of risk-stratifying. Coronary angiography is the diagnostic test of choice for patients with chest pain (angina) and signs of myocardial ischemia on noninvasive testing. Typically CAD is diagnosed based on the patency of the epicardial coronary arteries [1]. Approximately 30% of patients with angina have non-obstructive arteries on coronary angiogram and area diagnostic and management challenge for clinicians, contributing to signifcant social and economic burden [2]. They undergo multiple angiograms, experience a hospitalization rate 80% greater than patients with single vessel CAD and up to 50% have persistent symptoms leading to functional disability [3]. Historically, this population was given reassurance as long-term prognosis was believed to be benign [4]. We now know that a subset of these patients sui¬Â€er from coronary micro vascular dysfunction (MVD) [1] and are at increased risk for adverse cardiac events including congestive heart failure (CHF), myocardial infarction (MI), left ventricular (LV) dysfunction, and death [1,5]. The Cardiovascular Integrated Physiology (CVIP) program at Southlake Regional Health Centre (SRHC) investigates and manages patients with MVD. CVIP has received referrals for only a small fraction of patients with angina and non-obstructive angiograms at SRHC. It is unclear what factors promote referral. We hypothesized that referrals were not random and that the clinical characteristics of the referred patients dii¬Â€ered from the larger population of patients with angina and nonobstructive CAD. The primary objective of this study was to determine whether the patients referred to CVIP are an accurate representation of the overall population of patients with angina and non-obstructive coronary arteries.

Knockdown of p66ShcA activates Nrf2 pathway to protect cardiomyocytes from oxidative stress and inflammation induced by H2O2.

Oxidative stress and inflammation are the most common causes of myocardial ischemia and hypoxia. This article focuses on the effect of p66ShcA on H2O2-induced cardiomyocytes. The p66ShcA knockdown model of H9c2 cells was constructed by plasmid transfection. After treatment of different groups with H2O2, oxidative stress-related factors and inflammatory factors were detected. The expressions of SOD1, SOD2, GPX1, and GPX3 in H2O2 cells were significantly decreased, IL-1β and IL-6 expression were significantly increased, while p66ShcA siRNA negative group could promote the expression of SOD1, SOD2, GPX1, and GPX3, inhibit the expression of IL-1β and IL-6 significantly, and activates the Keap1/Nrf2 pathways. Knockdown of p66ShcA can activate Keap1/Nrf2 pathway, which inhibits H2O2-induced oxidative stress and inflammation in H9c2 cells.

Anabolic steroid excess and myocardial infarction: From ischemia to reperfusion injury

Anabolic steroids (AS) are synthetic testosterone-derivatives developed by the pharmaceutical industry to mimic testosterone biological effects. So far, AS have been implicated in the treatment of pathological conditions, such as hypogonadism, anemia, and cachexia. Since their discovery, though, AS have been illicitly used by elite and recreational athletes, bodybuilders and weightlifters in order to enhance athletic and aesthetic performance. This practice is characterized by cycles of administration and withdrawal, the combination of different AS compounds, and administration of doses 50 – 1000 times higher than those recommended for therapeutic purposes. AS excess has been correlated to cardiovascular detrimental effects, including cardiac hypertrophy, arrhythmias, and hypertension. Particularly, acute myocardial infarction (AMI) has been extensively reported by clinical and post-mortem studies. Atherosclerosis, hypercoagulability state, increased thrombogenesis and vasospasm have arisen as potential causes of myocardial ischemia in AS users. Additionally, several experimental reports have demonstrated that AS can increase the susceptibility to cardiac ischemia/reperfusion injury, whereas the cardioprotection elicited by physical exercise and ischemic postconditioning is blunted. Altogether, these factors can contribute to increased AMI morbidity and mortality during AS excess, particularly when AS are combined with other compounds, such as thyroid hormones, growth hormones, insulin, and diuretics.

Myocardial ischemia: From disease to syndrome

Although current guidelines on the management of stable coronary artery disease acknowledge that multiple mechanisms may precipitate myocardial ischemia, recommended diagnostic, prognostic and therapeutic algorithms are still focused on obstructive epicardial atherosclerotic lesions, and little progress has been made in identifying management strategies for non-atherosclerotic causes of myocardial ischemia. The purpose of this consensus paper is three-fold: 1) to marshal scientific evidence that obstructive atherosclerosis can co-exist with other mechanisms of ischemic heart disease (IHD); 2) to explore how the awareness of multiple precipitating mechanisms could impact on pre-test probability, provocative test results and treatment strategies; and 3) to stimulate a more comprehensive approach to chronic myocardial ischemic syndromes, consistent with the new understanding of this condition.

Dissecção coronária espontânea recorrente intra-hospitalar afetando diversas artérias

Spontaneous coronary artery dissection is an uncommon cause of myocardial ischemia. Although the first description dates from 1931, its diagnosis is sometimes made late and/or erroneously due to the lack of knowledge of its non-pathognomonic angiographic variations. Additionally, the proper management of this condition is not yet well established. Here we present a rare case of in-hospital recurrence of spontaneous dissection affecting both the left anterior descending and circumflex coronary arteries, with distinct clinical presentations. In-hospital recurrent spontaneous coronary [...]