The Incidence of Cardiovascular Events in Small Versus Large Ischemic Stroke; A Three-Year Cohort Study.

INTRODUCTION: Cerebral ischemia and coronary artery disease (CAD), the major leading causes of mortality and morbidity worldwide, are pathophysiologically interrelated. Cerebral ischemic events are categorized as large or small vessels disease. The current study compares the factors related to CAD events incidence following ischemic large versus small disease CVA. METHOD: The current cohort study was conducted on 225 patients with ischemic stroke in two groups of large (n=75) and small (n=150) vessel disease during 2018-19. The patients' demographic, medical, and clinical characteristics were recruited. They were followed for three years regarding the incidence of CAD events, including ST-elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), unstable angina (UA), and sudden cardiac death (SCD). Data about the coronary angiography, computed tomography angiography (CTA), Single Photon Emission Computed Tomography (SPECT), and the therapeutic approach were gathered. RESULTS: There were insignificant differences between the patients with small versus large vessels CVA in terms of ACS incidence (P-value=0.105), type of the events (P-value=0.836), angiographic (P-value=0.671), SPECT (P-value=0.99) and CTA findings (P-value>0.99) and approached CAD (P-value=0.728). Cox regression assessments revealed an increased risk of CAD events due to large versus small vessels disease after adjustments for hypertension, diabetes mellitus, dyslipidemia, re-stroke, and the previous history of IHD (HR=2.005, 95%CI: 1.093-2.988, P-value=0.021). CONCLUSION: According to the findings of this study, large-vessel involvement in an ischemic stroke was associated with more than a two-fold increase in the three-year probability of ischemic heart disease incidencet.

ncRNAs and polyphenols: new therapeutic strategies for hypertension.

Polyphenols have gained significant attention in protecting several chronic diseases, such as cardiovascular diseases (CVDs). Accumulating evidence indicates that polyphenols have potential protective roles for various CVDs. Hypertension (HTN) is among the hazardous CVDs accounting for nearly 8.5 million deaths worldwide. HTN is a complex and multifactorial disease and a combination of genetic susceptibility and environmental factors play major roles in its development. However, the underlying regulatory mechanisms are still elusive. Polyphenols have shown to cause favourable and beneficial effects in the management of HTN. Noncoding RNAs (ncRNAs) as influential mediators in modulating the biological properties of polyphenols, have shown significant footprints in CVDs. ncRNAs control basic functions in virtually all cell types relevant to the cardiovascular system and, thus, a direct link with blood pressure (BP) regulation is highly probable. Recent evidence suggests that a number of ncRNAs, including main small ncRNAs, microRNAs (miRNAs) and long ncRNAs (lncRNAs), play crucial roles with respect to the antihypertensive effects of polyphenols. Indeed, targeting lncRNAs by polyphenols will be a novel and promising strategy in the management of HTN. Herein, we reviewed the effects of polyphenols in HTN. Additionally, we emphasized on the potential effects of polyphenols on regulations of main ncRNAs, which imply the role of polyphenols in regulating ncRNAs in order to exert protective effects and thus proposing them as new targets for HTN treatment.Abbreviations : CVD: cardiovascular disease; BP: blood pressure; HTN: hypertension, lncRNAs: long noncoding RNAs; p38-MAPK: p38-mitogenactivated protein kinase; OPCs: oligomeric procyanidins; GTP: guanosine triphosphate; ROS: reactive oxygen species; cGMP: cyclic guanosine monophosphate; SGC: soluble guanylate cyclase; PI3K: phosphatidylinositol 3-kinase; cGMP: Cyclic GMP; eNOS: endothelial NO synthase; ERK ½: extracellular signal-regulated kinase ½; L-Arg: L-Arginine; MAPK: mitogen-activated protein kinases; NO: Nitric oxide; P: Phosphorus; PDK1: Phosphoinositide-dependent kinase 1; PI3-K: Phosphatidylinositol 3-kinase; PIP2: Phosphatidylinositol diphosphate; ncRNAs: non-protein-coding RNA; miRNAs: microRNAs; OPCs: oligomeric procyanidins; RES: resveratrol; GE: grape extract; T2DM: type 2 diabetes mellitus; IL: interleukin; TNF-α: tumour necrosis factor-alpha; NF-κB: nuclear factor NF-kappa-B; ALP: alkaline phosphatase; PARP1: poly [ADP-ribose] polymerase 1; HIF1a: Hypoxia-inducible-factor 1A; NFATc2: nuclear factor of activated T cells 2; PAD: peripheral artery disease; SHR: spontaneously hypertensive rat; RAAS: renin-angiotensin-aldosterone system; AT1R: angiotensin type-1 receptor; Nox: NADPH oxidase; HO-1: haem oxygenase-1; JAK/STAT: Janus kinase/signal transducers/activators of the transcription; PNS: panax notoginseng saponin; snoRNA: small nucleolar RNA; hnRNA: heterogeneous nuclear RNA; VSMCs: vascular smooth muscle cells; irf7: interferon regulatory factor 7; limo2: LIM only domain 2; GWAS: genome-wide association study; GAS5: Growth arrest-specific 5; Asb3, Ankyrin repeat and SPCS box containing 3; Chac2: cation transport regulator homolog 2; Pex11b: peroxisomal membrane 11B; Sp5: Sp5 transcription factor; EGCG: epigallocatechin gallate; ApoE: Apo lipoprotein E; ERK-MAP kinase: extracellular signal-regulated kinases-mitogen-activated protein kinase; PAH: pulmonary artery hypertension; PAP: pulmonary arterial pressure; HIF1a: hypoxia-inducible-factor 1A; NFATc2: nuclear factor of activated T cells 2; HMEC-1: Human microvascular endothelial cells; stat2: signal transducers and activators of transcription 2; JNK: c-Jun N-terminal kinase; iNOS: inducible NO synthase. SNP: single nucleotide polymorphism; CAD: coronary artery disease.