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Prayer, meditation and mindfulness have been commonly used for healing in Vedic, Jainism, Buddhism, Egyptian, Greek and Mesopotemian cultures [1]. In Buddhism, mindfulness is a component of Eight Fold Path, therefore using mindfulness in the modern science is not absolutely correct. A definition of prayers of Mesopotamia was “praise to god followed by request.” The ancient mystic Hinduism wrote Rigveda prayer, Figure 1.\ud Meditation and prayer appear to be important practices for the management of emotional and spiritual wellbeing [1-4]. Prayer may also influence the physiology of circadian rhythms in our body and it has evolved possibly as adaptation to the rotation of the earth around its axis [4]. Circadian rhythms account for increased activity of the sympathetic nerves of the autonomic nervous system with marked releases of cortisol, catecholamines (norepinephrine and adrenaline), testosterone and thyroid hormones. In turn, these neurotransmitters and hormones occur at a circadian stage when endogenous melatonin level is decreased to low values in the morning [4]. There is a need to prevent the circadian rhythm of adverse biological functions observed between 6.00 to 12.00 hours during the day, because circadian dysfunction can predispose to cardiovascular diseases (CVDs). The circadian dysfunction may worsen due to risk factors, although protective factors such as prayer, meditation and moderate physical activity may prevent circadian dysfunction [2-4]. The aim of the present study is to emphasize the beneficial role of prayer, mindfulness and meditation in the protection against circadian dysregulation in the body, thereby preventing CVDs, especially sudden cardiac death (SCD).

Circadian rhythm of increased oxidative stress and deficiency of antioxidant vitamins is known to occur in the morning at 6.00 hours to 12.00 hours [1]. Apart from antioxidant and vitamin deficiency, there is also deficiency of catalase, super-oxide-dismutase (SDO) and glutathione peroxidase (GPO) due to increased requirement of antioxidant enzymes in the morning. Methylglyoxal (MGO) is a non-enzymatic metabolite in the glycolytic pathway and its concentration in blood and tissues is elevated in all the cardio-metabolic diseases, including obesity and diabetes mellitus (DM) [1, 2]. MGO is a reactive carbonyl species (RCS) and in turn it induces tissue injuries via reactive oxygen species (ROS), resulting in increased damage of target tissues, which may worsen in the morning. MGO also plays an important pathological role in the development of both cardiovascular diseases (CVDs) and diabetes via the AGEs exert irreversible effects on protein structure and function. As such, it is crucial to understand the underlying mechanism whereby MGO is inducing tissue damage. This mini-review aims to highlight the role of circadian dysfunction in the pathogenesis of diabetes mellitus and its complications.

Obesity has become a public global health problem. More than 13% of the world’s 7.8 billion people (11% of men and 15% of women) are obese, defined as having a body mass index above 30 kg/m2. In North America and several Middle Eastern Countries, more than 30% of adults are obese. The alarming problem is that children as young as twelve years of age are now becoming obese. Obesity with high-fat and high-sugar diets is a risk factor for type 2 diabetes mellitus (T2DM), hypertension and early-onset heart failure (HF) with preserved ejection fraction (HFpEF) that leads to frequent hospitalizations. It is possible that diet, inactivity and other modern lifestyle factors may have an important role in the development of heart failure, either with or without decrease in ejection fraction [1]. This mini review discusses whether circadian oscillations in metabolism and inflammation could be responsible for the time-of-day-dependence of adverse cardio-vascular events in patients with HFpEF by increasing production of cytotoxic a-dicarbonyl species methylglyoxal (MG) and by decreasing expression of the primary MG-degrading enzyme glyoxalase-1 (Glo1), respectively.

The coronavirus 2 (SARS‐CoV‐2) induces severe acute respiratory distress syndrome (ARDS)via the coronavirus receptor angiotensin‐converting enzyme 2 (ACE2) in the host cell to facilitate entry into the lungs Over activation of the renin‐angiotensin system (RAS) and the down regulation of ACE2 expression are involved in SARS‐CoV induced lung injury. RAS is the main system that has a regulatory roleinmaintaining electrolyte balance, blood pressure, vascular tone and cardiovascular remodeling in the body. Angiotensin II receptor blockers (ARBs) and Inhibitors (ACEIs) are vital medications that are widely used for the treatment of cardiovascular diseases (CVDs). The question which now arises is: It is possible to continue using either ARBs or ACEIsor both medications in patients with SARS-CoV2? Both ARBs and ACEIs can facilitate COVID-19 entry into the host cell due to increase expression of ACE2. On the other hand, ARBs have a greater potential to reduce downstream pathogenicity of the SARS-CoV2 via different cell signaling pathways including free radical generation, up regulation of NF-κB pathway, toll-like receptors (TLRs) and pro-apoptotic protein by blocking the renin–angiotensin system more severely compared to the effect of ACEIs. The current hypothesis is that ARBs can perform better therapeutically compared to ACEIs in respiratory disorders such as ARDS which is induced by viral infection especially since more than 40 % of angiotensin II can be synthesized by other enzymes such as chymase, cathepsin. ARBs treatment can increase the levels of both angiotensin II (Ang II) and the ACE2 enzyme making Ang II a target substrate for hydrolysis by ACE2 into Ang 1-7 which in turn exerts anti-inflammatory, anti-apoptotic and anti-oxidant activities. These effects are achieved by the binding of Ang 1-7 to both angiotensin-type 2 receptor (AT2) and receptor mas’ axis (Mas) and also by its ability to block Ang II/AT1 receptor-induced TLR4/MyD88 signaling thereby highlighting the potential therapeutic use of ARB sin preventing injury induced by COVID-19 virus. It is concluded that patients who are already on ARBs medications must continue to use them daily since ARBs have protective effects against COVID-19 virus. Moreover, ARB sexert their beneficial effects via their anti-inflammatory, anti-apoptotic, anti-oxidant and anti-fibrotic properties. On the other hand, those patients who are on ACEIs medications must change to other safe drugs since ACEIs can facilitate an increase in COVID-19 virus entry into the body as well as reducing levels and protecting effect of Ang 1-7.

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.\ud 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.\ud Results. The results show that cardiac functions via conventional echocardiography (CE) were similar in the 2 groups. Using TDI and conventional mitral Doppler flow, obese subjects with diabetes showed an evidence of diastolic function abnormalities in the form of lower Ea velocity (9.5 ± 2.9 vs. 18.4 ± 3.5 cm/s, p < 0.0001), an increased Aa velocity (16.5 ± 2.4 vs. 14.1 ± 2.2 cm/s p < 0.05), higher left ventricular filling pressure (E/Ea = \ud 12 ± 4.4 vs 8±3.1), p < 0.05), as well as a reduced Ea/Aa ratio (1.00 ± 0.2 vs. 1.45 ± 0.3, p < 0.0001, in the study group versus control group. respectively. This study also showed that severely obese subjects (BMI >35) (n = 26) had reduced LV systolic and diastolic function compared with healthy controls. Regarding, systolic function indices, the findings revealed lower average longitudinal peak systolic strain, sm and reduced em, although, LV ejection fraction remained normal (56.48% ± 8.81). Among subjects with severe obesity (n = 26), the findings reveal that global longitudinal presystolic strain (GLPSS) is highly correlated with maximum rate of pressure development of LV (dp/dt), although the LVEF remained normal, in comparison to systolic strain and dp/dt. (.5% ±1.4 vs -19.54% ± 4.5; \ud p < 0.001), in the age-matched healthy subjects. However, the frequency/grade of DCM detected by STE, among patients having obesity with T2DM, correlated closely with the degree of obesity, metabolic abnormalities and clustering of other major risk factors, especially high blood pressure. The findings also revealed that chest pain due to coronary heart disease (CAD), dyspnea and DCM were more common among female patients compared to men.\ud Conclusion. The results indicate that patients having obesity with T2DM should be advised to undertake early TDI and STE for early diagnosis of decreased cardiac diastolic and systolic dysfunctions and cardiomyopathy, which is likely to be missed by conventional echocardiography. Significant differences in regional and global strain were also identified between the severely obese diabetic (BMI ≥ 35), (GLPSS (-13) patients compared to less obese subjects.

Hypertensive Cardiomyopathy (HTN-CM) is a structural cardiac disorder generally accompanied by concentric or eccentric Left Ventricular Hypertrophy (LVH) associated with diastolic or/and systolic dysfunction in patients with persistent systemic hypertension. It occurs in the absence of other cardiac diseases capable of causing myocardial hypertrophy or cardiac dysfunction. Long standing arterial hypertension (HTN) leads to structural and functional myocardial abnormalities resulting in myocardial ischemia, fibrosis, and hypertrophy. HTN-CM is predominantly a disease of impaired relaxation rather than impaired contractility, although subtle myocardial systolic abnormalities could be detected recently by Global Longitudinal Systolic Strain (GLS) Speckle Tracking Echocardiography (STE). Importantly, the accompanying LVH is itself a risk factor for mortality and morbidity and is considered an independent predictor for Sudden Cardiac Death (SCD). Therefore, early detection of LVH development in patients with Hypertensive Hypertrophic Cardiomyopathy (HTN-CM) is crucial for optimal treatment. In addition to pathological findings, echocardiography and cardiac magnetic resonance imaging are ideal tools for the diagnosis of HTN-CM and can differentiate it from Hypertrophic Cardiomyopathy (HCM). Timely diagnosis of this condition and utilization of appropriate treatment are required to improve morbidity and mortality in hypertensive patients. This review presents an overview of utilization of multidisciplinary imaging modalities approach for proper diagnosis of HTN-CM and its differentiation from HCM. Relevant article highlighted key points in differentiation of HTN-CM from HCM and the effects of hypertension on cardiac hypertrophy and heart failure development are discussed in clinical case study.