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Background. Obesity and type 2 diabetes mellitus (T2DM) are two interrelated and preventable disorders. However, they are responsible for significant global mortality from cardiovascular diseases (CVDs). Clinical studies have demonstrated that global longitudinal strain (GLS) using speckle tracking echocardiography (STE), can assess myocardial function accurately in apparently, healthy patients with diabetes and obesity in the settings of acute and chronic ischemia and suspected cardiomyopathy without heart failure. No such studies have been published to date regarding subclinical detection of cardiac dysfunction among obese patients with T2DM. This study aims to investigate the role of STE in the early pre-clinical diagnosis of impairment of diastolic and systolic dysfunction in obese patients with T2DM. This study also investigated whether it is possible to detect early pre-clinical impairment of diastolic and systolic dysfunction in obese T2DM patients, via Tissue Doppler Imaging (TDI), maximum rate of left ventricular pressure development (peak dP/dt) and GLS using STE for comparison. Subjects and Methods. After clearance from the review board of Dibba- Hospital, Alfujairah, UAE, all the available records of patients with the diagnosis of obesity and diabetes were examined. The study included 214 patients presenting with obesity in conjunction with diabetes and 93 age-matched healthy control subjects. STE was performed among all the patients and subjects along with Tissue Doppler Imaging (TDI). This study assessed maximal rate of pressure rise during ventricular contraction (peak dP/dt) and global longitudinal strain (GLS) using STE methods. Transthoracic echocardiography, myocardial Doppler-derived systolic (sm), early diastolic velocity (em) and GLS were also obtained, among all the subjects. Results. The results show that cardiac functions via conventional echocardiography (CE) were similar in the 2 groups. Using TDI and conventional mitral Doppler flow, obes

Background: Acute kidney injury (AKI) is an important and one of the most common complications after acute myocardial infarction (AMI), affecting from 10 to 55% of patients globally. However, the mechanisms causing AKI in the first few days after an AMI are multi-factorial in nature. Recent studies suggest that AKI is associated with poor outcomes and independently predicts increasing long-term mortality. However, few studies have investigated the early risk of AKI with AMI. Patient and methods: This was a cross-sectional study involving 110 patient with acute ST elevation during AMI. Those patients who were admitted to the coronary care unit were examined to see if they developed AKI. Complete clinical studies were carried out during the patients’ hospital stay. AKI was defined as an increase in SCr by ≥0.3 mg/dl within 48 h or an increase in SCr to ≥ 1.5 times baseline within the first 7 days of hospitalization (based on the KDIGO criteria). Results: AKI occurred in 14 of the 110 (12.7%) patients; with 8 patients (57%) of AKI in stage 1 and 4 patients (29%) in stage 2 and 2 patients (14%) in stage 3. Patients who developed AKI were significantly more likely to be older, have hypertension, previous CAD, and diabetes mellitus than the non-AKI patients (p < 0.05 for all comparisons). Patients with AKI were significantly more likely to receive diuretics than non-AKI patients (p < 0.00052). Patients with anterior STEMI significantly developed AKI more than other type of MI (p < 0.015). Mortality was found more among STEMI patients who developed AKI (p < 0.0223). AKI in STEMI patients was more prevalent in those patients with increased serum creatinine (p < 0.047) and decreased eGFR (p < 0.0001) at time of admission. Conclusion: AKI occurred in 12.7% (14/110) of patients hospitalized for acute STEMI. This common complication was strongly associated with mortality. The presence of a low eGFR level on admission in patients with AMI-associated AKI was related to a poor sho

Background and aims: Early detection of coronary artery disease (CAD) in patients with non-ST elevation acute coronary syndrome (ACS) remains a clinical challenge, especially in the absence of regional wall motion abnormalities by echocardiography on presentation. This study was designed to evaluate the accuracy of Global Longitudinal Strain (GLS) by speckle tracking analysis for the diagnosis of significant CAD in patients with ACS. It also assessed the ability of Territorial Longitudinal Strain (TLS) analysis in localizing the coronary artery lesion, along with coronary angiography (CA), considered the gold standard. Patients and Methods: This study included 133 patients who presented with non-ST elevation acute coronary syndrome (NSTEACS) to the emergency department, Heart Hospital, Hamad Medical Corporation, Doha, Qatar, during the period of January 1, 2014 to May 31, 2015. 85% of the patients were male; they ranged in age from 32 to 65 years (mean ± SD: 49.4 ± 9.5 years). Significant CAD was defined as having at least one epicardial vessel with ≥ 70% or left main > 50% stenosis. All patients enrolled in this study underwent basic echocardiography, speckle tracking analysis, and coronary angiography. Results: The echocardiogram obtained from the patients did not show any wall motion abnormalities at rest, although speckle tracking analysis was abnormal in 97 patients. Average GLS was considered positive for CAD if ≥ -18.7%. TLS was also calculated for each major artery, as the average of the strain of the segments supplied by that artery. TLS was considered positive if ≥ -16.7%. In other experiments, GLS and TLS were compared with CA results. Here, the patients were further subdivided into those with either multi-vessel disease or left main disease (MV, n = 52, 53.6%), and those with single vessel disease (SV, n = 45, 46.4%). LAD, circumflex and RCA lesions were found in 65, 50 and 39 patients, respectively. A control group of 29 cases was selected from outpatie

Sudden cardiac death (SCD) is a sudden unexpected death due to a demise of the myocardium. SCD also includes an acute precipitating trigger that lies in the brain and a chronic electrical instability of the myocardium. Most SCDs in absolute terms occur in subjects with no known pre-existing heart disease. The incidence of SCD may be about 20% per year in patients with heart failure and those with markers of arrhythmias, compared with about 1-2% in the general population, i.e., subjects with no “known” pre-existing heart disease. Some early symptoms of SCD include fatigue, fainting, blackouts and dizziness due to blood stopping to flow to the brain and other organs of the body. SCD is responsible for a sizable portion of the over 19 million deaths globally each year from CVDs. Acute anxiety, hypertension, hyperlipidemia, family history, arrhythmias, diabetes mellitus, prediabetes, metabolic syndrome and obesity are risk factors to precipitate SCD. In addition, other behavioral risk factors including type A personality, physical inactivity, smoking, male gender, women after menopause, unhealthy diet and modern lifestyle, such as regularly eating fast foods or foods rich in saturated fats, and late-night sleep; excess sugar, alcohol and salt intake can also predispose to SCD. Deficiency in some cations and vitamins, especially magnesium, potassium, flavonoids and trace elements, and thiamine, have been associated with SCD. One or a combination of these risk factors can lead to pathological conditions and cardiovascular diseases (CVDs) that predispose to SCD. The most common physio-pathological event is the rupture of the vulnerable atherosclerotic plaque with athero-thrombosis, observed in the majority of the patients with acute coronary syndromes (ACSs) and SCD. In an animal experiment, it has been reported that neutrophil-depleted animals had worsened cardiac function, increased fibrosis, and progressively developed heart failure, indicating that high neutrophil coun

Detecting genetic risk factors for better targeting of statin administration can further enhance the benefit of this therapy. Coronary artery disease (CAD) is a polygenic disorder with multiple genetic variants. A composite of some of these variants could ascertain the risk of both incident and recurrent CAD events and help in the diagnosis of patients at greater risk who could get greater clinical benefit from statin treatment [1]. The role of genetic risk factors in CAD has become more relevant with the discovery of the proprotein convertase subtilisin kexin type 9 (PCSK9) enzyme, which is responsible for regulating cholesterol metabolism [2, 3]. Gain-of-function mutations of the PCSK9 gene may be associated with increased cholesterol and increased risk of CVDs, whereas loss-of-function mutations are linked to lower blood cholesterol and a reduction of CVDs risk without any known adverse effects [2-5]. This included a community-based landmark assessment employing multiple studies involving 48,421 individuals and 3,477 events [1]. This analysis examined the association of a genetic risk score based on 27 genetic variants with either incident or recurrent CAD, adjusting for traditional clinical risk factors. All subjects were divided into low (quintile 1), intermediate (quintiles 2–4), and high (quintile 5) genetic risk categories, to demonstrate a significant gradient in risk for incident or recurrent CAD. The multivariable-adjusted hazard ratio for CAD events for the intermediate genetic risk category was 1.34 (95% CI: 1.22–1.47, p < 0.0001) and that for the high genetic risk category was 1.72 (1.55–1.92, p < 0.0001) compared with the low genetic risk subjects [1]. There was a significant gradient (p = 0.0277) of increasing relative risk across the low (13%), intermediate (29%), and high (48%) genetic risk categories. Absolute risk reduction from statin treatment was greater in some patients with higher genetic risk categories (p = 0.0101). In the primary preventi