Atherosclerosis preventive effects of marrubiin against (TNF-α)-induced oxidative stress and apoptosis.

Introduction: Atherosclerosis is a complicated cascade of inflammatory processes, oxidative stress, and apoptosis, making it the most prevalent cardiovascular disease. The onset and progression of cardiovascular diseases are greatly influenced by oxidative stress. Targeting oxidative stress is an effective strategy for treating such diseases. Marrubiin is a bioactive furan labdane diterpenoid acts as a strong antioxidant to protect against oxidative damage. This study aimed to investigate the protective effects of marrubiin against oxidative stress and apoptosis in a cellular model of the vascular system. Methods: Human umbilical vein endothelial cells were treated with varying concentration of marrubiin and its IC50 value was determined. The antioxidant potential of marrubiin was assessed by measuring the intracellular level of glutathione (GSH) using a colorimetric technique. Since apoptosis plays a significant role in the plaque rupture, the study also evaluated the protective effects of marrubiin on the expression of key genes involved in apoptotic pathways. Results: Cells treated with marrubiin showed increased GSH levels compared to cell therapy control cells, indicating marrubiin's ability to counteract the effects of TNF-α's on GSH levels. Furthermore real-time PCR analysis demonstrated that marrubiin upregulated Bcl-xl while downregulating caspase3 and Nox4 in treated cells. These findings suggest that marrubiin protects against apoptosis and oxidative stress. Conclusion: Based on our findings, marrubiin is recommended as a preventive/therapeutic treatment for diseases caused by elevated intracellular reactive oxygen species levels in cardiovascular diseases.

Forskolin Improves Male Reproductive Complications Caused by Hyperglycemia in Type 2 Diabetic Rats.

BACKGROUND: In many diabetic patients, spermatogenesis complications are frequent causing infertility problems. This study aimed to demonstrate the effect of Forskolin on male reproductive dysfunction caused by type 2 diabetes. MATERIALS AND METHODS: In this experimental study, type 2 diabetes was induced by a high-fat diet (HFD) for one month and then a low single dose injection (35 mg/kg) of streptozotocin (STZ) in Wistar rats. After 72 hours, rats with more than 200 mg/dl of blood glucose were considered type 2 diabetic rats. Forty rats (200-250 g) were divided into four groups (n=10) including group 1 (G1): rats with normal diet and buffer citrate (STZ solvent) injection, group 2 (G2): control type 2 diabetic rats with HFD and STZ injection, group 3 (G3): type 2 diabetic rats received phosphate buffer saline (PBS) as Forskolin solvent, and group 4 (G4): Forskolin treated diabetic rats (10 mg/kg) for 1 month. RESULTS: In comparison to control group, in diabetic groups (G2 and G3) some parameters are increased significantly: The blood glucose (P=0.00078), testicular malondialdehyde (MDA) level and body weight (P=0.00009) and Bax gene expression (P=0.00007). Unlike, some parameters are decreased significantly: The serum level of testosterone (P=0.0009), testicular superoxide dismutase (SOD, P=0.00007) and glutathione peroxidase (GPX) levels (P=0.00008), sperm concentration (P=0.00008), motility (P=0.00009), normal morphological sperm (P=0.00008) and Bcl-2 gene expression (P=0.00009). However, in Forskolin treated group (G4) the parameters stayed close to control values that was significantly (P=0.00007) higher than in G2 and G3 groups. Therefore, treatment with Forskolin significantly improved these abnormal changes in Forskolin-treated group. CONCLUSION: Our study demonstrates that Forskolin is an effective antidiabetic agent, which significantly improves sperm concentration, testosterone levels, and antioxidant activity in diabetic rats.

Long and Short-term Metformin Consumption as a Potential Therapy to Prevent Complications of COVID-19.

Purpose: The aim of the study is to evaluate the effect of metformin in complication improvement of hospitalized patients with COVID-19. Methods: This was a randomized clinical trial that involved 189 patients with confirmed COVID-19 infection. Patients in the intervention group received metformin-500 mg twice daily. Patients who received metformin before admission were excluded from the control group. Patients who were discharged before taking at least 2000 mg of metformin were excluded from the study. Primary outcomes were vital signs, need for ICU admission, need for intubation, and mortality. Results: Data showed that patients with diabetes with previous metformin in their regimen had lower percentages of ICU admission and death in comparison with patients without diabetes (11.3% vs. 26.1% (P=0.014) and 4.9% vs. 23.9% (P≤0.001), respectively). Admission time characteristics were the same for both groups except for diabetes and hyperlipidemia, which were significantly different between the two groups. Observations of naproxen consumption on endpoints, duration of hospitalization, and the levels of spO2 did not show any significant differences between the intervention and the control group. The adjusted OR for intubation in the intervention group versus the control group was 0.21 [95% CI, 0.04-0.99 (P=0.047)]. Conclusion: In this trial, metformin consumption had no effect on mortality and ICU admission rates in non-diabetic patients. However, metformin improved COVID-19 complications in diabetic patients who had been receiving metformin prior to COVID-19 infection, and it significantly lowered the intubation rates.

Toll-Like Receptor 4 (TLR4) and AMPK Relevance in Cardiovascular Disease.

Toll-like receptors (TLRs) are essential receptors of the innate immune system, playing a significant role in cardiovascular diseases. TLR4, with the highest expression among TLRs in the heart, has been investigated extensively for its critical role in different myocardial inflammatory conditions. Studies suggest that inhibition of TLR4 signaling pathways reduces inflammatory responses and even prevents additional injuries to the already damaged myocardium. Recent research results have led to a hypothesis that there may be a relation between TLR4 expression and 5' adenosine monophosphate-activated protein kinase (AMPK) signaling in various inflammatory conditions, including cardiovascular diseases. AMPK, as a cellular energy sensor, has been reported to show anti-inflammatory effects in various models of inflammatory diseases. AMPK, in addition to its physiological acts in the heart, plays an essential role in myocardial ischemia and hypoxia by activating various energy production pathways. Herein we will discuss the role of TLR4 and AMPK in cardiovascular diseases and a possible relation between TLRs and AMPK as a novel therapeutic target. In our opinion, AMPK-related TLR modulators will find application in treating different immune-mediated inflammatory disorders, especially inflammatory cardiac diseases, and present an option that will be widely used in clinical practice in the future.

Effects of pre-treatment with metoprolol and diltiazem on cerebral ischemia/reperfusion-induced injuries

Abstract Stroke is one of the most important health concerns worldwide. Calcium ions accumulation in the nerve cells and increase in the catecholamines level of the brain following cerebral ischemia/reperfusion (I/R) are accompanied by damaging effects. Therefore, the present study aimed to evaluate the effects of diltiazem, as a calcium channel blocker, and metoprolol, as a β-adrenoceptors antagonist, on I/R injury. In this study, 30 male Wistar rats were divided into control, I/R, metoprolol, diltiazem, and metoprolol plus diltiazem groups (n=6 in each). Metoprolol (1 mg/kg/day) and diltiazem (5 mg/kg/day) were injected intraperitoneally (i.p.) for 7 days before I/R induction. On day 8, the animals underwent ischemia by bilateral common carotid arteries occlusion for 20 min. Histopathological analysis showed a significant reduction in leukocyte infiltration in diltiazem, metoprolol, and diltiazem plus metoprolol treated rats compared with the I/R group (P<0.05, P<0.01, P<0.01, respectively). In addition, in all treated groups, myeloperoxidase activity and malondialdehyde levels in the brain tissue significantly declined compared with the I/R group (P<0.001). Furthermore, pre-treatment with diltiazem and metoprolol alone or in co-administration remarkably reduced infarct size following I/R (P<0.001). Overall, the results indicate the considerable neuroprotective effects of metoprolol and diltiazem in cerebral I/R.

Time-dependent influence of infliximab on hemodynamic responses and cardiac injuries of isoproterenol-induced myocardial infarction in rats.

Immune-induced inflammation plays an important role both in aggravating and healing of post myocardial infarction (MI) injuries. Potent anti-inflammatory and local immunomodulatory activity of infliximab has been suggested to have modulating effects on immune responses after MI. The aim of the present study was to evaluate the efficacy of infliximab on hemodynamic responses and myocardial injuries following isoproterenol-induced myocardial infarction. Male Wistar rats, weighting 260 ± 20 g were assigned into ten groups (n = 6) of saline (normal saline), infliximab (7 mg/kg), isoproterenol (100 mg/kg for two consecutive days), and isoproterenol plus infliximab (30 min after the second injection of isoproterenol). The heart tissues and serums were analyzed 24, 48, 72, and 96 h post-MI and hemodynamic parameters, histopathological changes, malondialdehyde (MDA), Total antioxidant capacity (TAC), lactate dehydrogenase (LDH), and lactate levels were assessed in the respective groups. Infliximab partially improved hemodynamic depression in the first days after MI, but the heart became more suppressed later. A similar result also obtained at the MDA tissue levels but not serum levels. Anti-inflammatory effects of Infliximab may improve cardiac function and prevent heart tissue injury early after MI; however, it can worsen the condition later by inhibiting compensatory reactions such as cardiac remodeling and tissue repair.

Erratum: Correction of Title.

[This corrects the article DOI: 10.15171/apb.2018.012.].

Effect of tetracycline on IL-1ß and IL-6 levels of the peri-implant sulcular fluid.

Background: Inflammation in the implant-abutment interface is one of the main factors that can reduce implant stability. Therefore, this study investigated the effect of chlorhexidine, tetracycline, saliva, and a dry environment on the interleukin IL-1ß and interleukin IL-6 levels of the gingival groove fluid at the implant-abutment interface. Methods: Twenty-four (10 men and 14 women) patients referred to the Faculty of Dentistry for implant treatment, who met the inclusion criteria, were examined. Four different materials were used in each implant, including 2% chlorhexidine, 3% tetracycline, saliva, and a dry medium. Each test material was placed inside the implant screw during the anchorage session, and the healing screw was closed. Patients were then sampled in three implantation sessions and one month after prosthesis delivery. Interstitial fluid groove was used for sampling after cleaning the mouth (half an hour after three minutes of thorough brushing). The data were analyzed with SPSS 20 using ANOVA and relevant post hoc tests. Results: There was a significant difference in the mean IL-6 and IL-1ß levels between the four materials (P<0.05). IL-6ß levels were similar in tetracycline and chlorhexidine but significantly higher than in saliva and the dry environment (P<0.05). IL-6 and IL-1ß levels in the saliva were significantly higher than in the dry environment (P<0.05). Conclusion: The use of tetracycline at the junction of implant and abutment reduces the inflammatory cytokines IL-6 and IL-1ß.

Oxidative stress and its association with ST resolution and clinical outcome measures in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention.

OBJECTIVE: Reperfusion of ischemic myocardium generates oxidative stress, which itself can mediate myocardial injury. So, in this study, we investigated the level of oxidative stress markers and its association with clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention. RESULTS: As indicated in the results, Post MI (Myocardial Infarction) heart failure was significantly higher in the group A (11% vs 4%, p = 0.047). Complete STR (ST-segment resolution) was observed to be significantly higher in the group B (36% vs 17%, p = 0.006). The SOD (Superoxide dismutase) and GPX (Glutathione peroxidase) levels were significantly higher in the group B compared to the other group (1547.51 ± 328.29 vs. 1449.97 ± 246.06, p = 0.019 and 60.62 ± 11.95 vs 57.41 ± 10.14, p = 0.042). The levels of GPX and SOD were shown to be directly related with complete STR and post PCI (Percutaneous coronary intervention)TIMI(Thrombolysis in Myocardial Infarction) flow 3 in the group A (p = 0.002 and p < 0.01, p = 0.005 and p < 0.02, respectively).

Oxidized cholesterol exacerbates toll-like receptor 4 expression and activity in the hearts of rats with myocardial infarction.

Introduction: The present study examined the effects of high cholesterol and high oxidized-cholesterol diets on the myocardial expression of TLR4 and pro-inflammatory cytokine in rats. Methods: Male Wistar rats were allocated into 6 groups and fed with a normal diet, cholesterol, and oxidized-cholesterol rich diets with or without isoproterenol-induced myocardial infarction. TLR4 and MyD 88 expression and levels tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) were measured in the heart and serum. Results: Oxidized cholesterol-fed animals had higher serum levels of oxidized low-density lipoprotein (LDL) (263 ± 13 ng/dL) than the cholesterol-fed animals (98 ± 8 ng/dL; P < 0.001). A high level of oxidized-LDL caused fibrotic cell formation and enhanced neutrophil infiltration in the absence of MI. Both cholesterol and oxidized-cholesterol upregulated TLR4 mRNA expression and increased TNF-α and IL-6 production in the hearts of rats with MI. In rats fed with oxidized-cholesterol the serum and myocardial levels of TNF-α (653 ± 42 pg/mL, 1375 ± 121 pg/100 mg, respectively) were higher than MI group (358±24 pg/mL, P < 0.001 and 885 ± 56 pg/100 mg, P < 0.01). A significant correlation was seen between TLR4 expression and infarct size. Conclusion: These findings suggest that cardiac TLR4 is preferentially upregulated by oxidized cholesterol in rats. Oxidized cholesterol may have a critical role in cardiac toxicity in the absence of pathological conditions.

Coenzyme Q10 in association with metabolism-related AMPK/PFKFB3 and angiogenic VEGF/VEGFR2 genes in breast cancer patients.

Low levels of coenzyme Q10 (CoQ10) have been reported in the circulation of patients with breast cancer, particularly in metastatic features. Our objective was to study the correlation between plasma levels of CoQ10 and the tumoral expression levels of AMPK, PFKFB3, VEGF, and VEGFR2. This study was a part of consecutive case series conducted on 100 women with newly diagnosed invasive ductal breast carcinoma, with an age range of 30-60 years. Plasma levels of CoQ10 were measured using HPLC coupled to an UV detector. The expression levels were quantified using quantitative real-time PCR. Structural equation modeling (SEM) was applied to generate pathways describing gene-to-gene inter-correlations. Using SEM identified AMPK expression to contribute positively to VEGF-A/VEGFR2 ratio (coefficient b = 0.64, P < 0.001). The VEGFR2 expression positively correlated with tumor size (coefficient b = 0.31, P < 0.001). A linear correlation between expression levels of AMPK and PFKFB3 was observed (rAdj = - 0.273, P = 0.02). Similarly, VEGF-A was correlated with VEGFR2 (rAdj = 0.698, P < 0.001). There were inverse significant correlations between CoQ10 and the fold changes of AMPK (rAdj = - 0.276, P = 0.030), VEGF-A (rAdj = - 0.319, P = 0.011) and VEGFR2 (rAdj = - 0.262, P = 0.045). The correlation between CoQ10 and the fold changes of PFKFB3 was significantly progesterone receptor (PR) dependent (rAdj = - 0.284, P = 0.041). Plasma CoQ10 was correlated with VEGF-A in hormone receptor-dependent mode (ER + : rAdj = - 0.286, P = 0.032 and PR + : rAdj = - 0.313, P = 0.025). Our findings could provide new insights suggesting CoQ10 can inversely correlate to the expression levels of VEGF-A/VEGFR2 as angiogenic factors and AMPK/PFKFB3 as biomarkers for tumoral glycolysis, especially in a hormone receptor-dependent manner to possibly prevent the progression of breast carcinogenesis.

Metformin Effect on Endocan Biogenesis in Human Endothelial Cells Under Diabetic Condition.

BACKGROUND AND AIM: Endocan is a novel endothelium-derived proteoglycan and may play a role in endothelial cells activity under diabetic conditions. Here, we evaluated the effect of high glucose concentration (30 mmol glucose) on endocan level in presence or absence of metformin in human umbilical vein endothelial cells (HUVECs). METHODS: Cells were incubated with 30 mmol glucose for 72 h. High glucose content, metformin (2.5 to 500 mmol) and compound C (10 mmol) effects were assessed on cell viability. HUVECs migration was studied by scratch test. The changes in endocan expression and protein level were evaluated by RT-PCR, ELISA and flow cytometry assays. Griess reaction was used to measure NO levels. Functional activity of endothelial cells was monitored related to lipoprotein lipase activity using Dil-Ac-LDL uptake. p-AMPK/AMPK ratio was assessed by western blotting. RESULTS: Cells viability significantly was reduced under high glucose condition (p <0.05). 30 mmol glucose inhibited HUVECs migration, whereas these features were improved by 50 mmol metformin (p <0.05). Endocan transcription and protein levels were increased in diabetic HUVECs exposed to metformin (p <0.05). Metformin increased NO production in HUVECs under high glucose condition (p <0.001). Metformin increased LDL uptake capacity under high glucose condition (p <0.05). The addition of compound C blunted these effects. Western blot analysis confirmed the increase of p-AMPK/AMPK ratio in metformin-treated cells. CONCLUSION: Data demonstrated that metformin could promote angiogenic potential of endothelial cells which its reduction is a main cause in the development of diabetic foot ulcer, probably by the regulation of endocan dynamics under high glucose condition.

Physicochemical and pharmacological evaluation of carvedilol-eudragit® RS100 electrosprayed nanostructures.

OBJECTIVES: This study was carried out to boost the pharmacologic influence of carvedilol (CAR) (as a poorly water-soluble drug) by developing CAR-eudragit® RS100 (Eud) nanofibers and nanobeads benefiting an electrospraying approach. MATERIALS AND METHODS: CAR-Eud nanoformulations with varying ratios (1:5 and 1:10) at total solution concentrations of 10 %, 15 % and 20 % w/v were formulated. RESULTS: The solution concentration remarkably impressed the size and morphology of the samples; in which, the nanobeads (mean diameter of 135.83 nm) were formed at low solution concentrations and high concentrations led to nanofibers (mean diameter of 193.45 nm) formation. DSC thermographs and PXRD patterns along with FTIR spectrum precisely showed CAR amorphization and no probable chemical interactions between CAR and Eud in the electrosprayed nanosystems. The in vitro release considerations demonstrated that the nanoformulations with the drug: polymer ratios of 1:10 and 1:5 depict rapid dissolution rate compared to the physical mixtures (PMs) and the pure drug. The in vivo studies in Wistar male rats suggested that the electrosprayed nanoformulation (1:10; 20 %) reduced the isoproterenol (ISO) induced elevation of heart rate, necrosis and accumulation of neutrophils in the heart tissue more efficient than the pure drug and PM. CONCLUSION: Our finding illustrated that the electrospraying as a profitable one-step procedure could be productively benefited to improve the physicochemical features and pharmacologic influences of CAR.

Severe complications of tramadol overdose in Iran.

OBJECTIVES: Severe complications of tramadol overdose have been reported; however, few large-scale studies have investigated this issue. Therefore, this study aimed to explore the presentation and complications of tramadol overdose in patients admitted to an intoxication referral center in northwestern Iran. METHODS: Patients with tramadol overdose admitted to Sina Teaching Hospital in Tabriz, Iran during 2013-2017 were included. For each patient, the following data were collected: demographics, previous drug or medication overdose, whether the patient was in the process of quitting drug use, ingested dose of tramadol and co-ingestants, Glasgow Coma Scale (GCS) score, clinical symptoms at the time of admission, and admission characteristics. Serotonin toxicity was diagnosed in patients who fit the Hunter criteria. Multiple logistic regression was performed to identify variables associated with the incidence of severe complications of tramadol overdose. RESULTS: In total, 512 cases of tramadol overdose were evaluated, of which 359 patients were included, with a median age of 41 years (range, 16-69) and a median tramadol dose of 1,500 mg (range, 500-4,000). The most frequent complications associated with tramadol overdose were hypertension (38.4%), tachycardia (24.8%), and seizure (14.5%). No serotonin toxicity was detected in patients. Having a GCS score <15, having taken a tramadol dose of >1,000 mg, being in the process of quitting drug use, being 30-49 years old, and male sex were significantly related to the incidence of severe complications of tramadol overdose. CONCLUSIONS: Although seizure was prevalent among Iranian patients with tramadol poisoning, serotonin toxicity and cardiogenic shock were rare findings.

Quercetin alleviates high glucose-induced damage on human umbilical vein endothelial cells by promoting autophagy.

BACKGROUND: Quercetin, a flavonoid antioxidant, has been found to exert therapeutic effects in diabetic condition. Autophagy represents a homeostatic cellular mechanism for the turnover of unfolds proteins and damaged organelles through a lysosome-dependent degradation manner. We speculated that quercetin could protect endothelial cells against high glucose-induced damage by promoting autophagic responses. METHODS: HUVECs viability was evaluated by MTT method. Griess and TBARS assays were used to monitor the levels of NO and MDA, respectively. Intracellular ROS generation was determined in DCFDA-stained cells analyzed by flow cytometry. To investigate the role of quercetin in endothelial cell migratory behavior, we used a scratch test. The level of autophagy proteins LC3, Beclin-1 and P62 were measured by western blotting technique. RESULTS: Our results showed that quercetin had the potential to increase cell survival after exposure to high glucose (P < 0.05). Total levels of oxidative stress markers were profoundly decreased and the activity of GSH was increased by quercetin (P < 0.05). High glucose suppressed HUVECs migration to the scratched area (P < 0.05). However, a significant stimulation in cell migration was observed after exposure to quercetin (P < 0.05). Based on data, autophagy was blocked at the late stage by high glucose concentration while quercetin enhanced autophagic response by reducing the P62 level coincided with the induction of Beclin-1 and LC3-II to LC3-I ratio (P < 0.05). All these beneficial effects were reversed by 3-methyladenine as an autophagy inhibitor. CONCLUSION: Together, our data suggest that quercetin could protect HUVECs from high glucose induced-damage possibly by activation of the autophagy response.

Predictive Value of Endocan Based on TIMI Risk Score on Major Adverse Cardiovascular Events After Acute Coronary Syndrome.

We assessed the prognostic value of serum levels of endocan in patients with the acute coronary syndrome (ACS) through its correlation with the Thrombolysis in Myocardial Infarction (TIMI) risk score and compared the possible association with clinical outcomes. In this prospective cross-sectional study, we enrolled 320 patients with documented ST-segment elevation myocardial infarction (STEMI), non-STEMI (NSTEMI), or unstable angina (UA) who underwent diagnostic coronary angiography. Endocan was measured soon after admission in the emergency department. In-hospital death, heart failure, and recurrent infarction were considered major adverse cardiac events (MACEs). There was a significant positive correlation between endocan level and TIMI risk score and MACE. The optimal cutoff values of endocan to predict clinical end points were 3.45 ng/mL in patients with STEMI and 2.85 ng/mL in patients with UA/NSTEMI. Multivariate logistic regression analysis indicated that endocan independently correlated with MACE. Moreover, cardiac troponin I, creatine kinase-MB, and circulating endocan were found to be independently associated with MACE in patients with ACS. In conclusion, a high endocan level on hospital admission is an independent predictor of worse cardiovascular outcomes and higher TIMI risk score in patients with ACS.

Prognostic Value of sLOX-1 Level in Acute Coronary Syndromes Based on Thrombolysis in Myocardial Infarction Risk Score and Clinical Outcome.

BACKGROUND: Biomarkers possess important diagnostic and prognostic value in acute coronary syndromes (ACSs). Soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1) is one of the markers involved in atherosclerotic plaque vulnerability and rupture. OBJECTIVE: This study aimed to evaluate the prognostic value of sLOX-1 through its correlation with Thrombolysis in Myocardial Infarction (TIMI) risk score and its possible association with clinical outcomes in 2 major spectrums of ACS. METHODS: A prospective cross-sectional study was planned, and 320 patients who underwent diagnostic coronary angiography were selected (in first 24 h after coronary angiography): those with documented ST elevation myocardial infarction or unstable angina/non-ST elevation myocardial infarction. sLOX-1 was measured immediately after administration in the emergency department. The TIMI risk score was calculated separately for both groups. In hospital death, heart failure and recurrent infarction were considered major adverse cardiac events. RESULTS: There was a significant positive correlation between sLOX-1, TIMI risk score, major adverse cardiac events, and heart failure. The optimal cutoff value of sLOX-1 to predict clinical endpoints was 1.75 ng/mL in patients with ST elevation myocardial infarction and 1.35 ng/mL in patients with unstable angina/non-ST elevation myocardial infarction. CONCLUSIONS: Circulating sLOX-1 could be used as a biomarker to predict major adverse cardiac events in patients with ACS and may be clinically useful in the triage and management of these patients.

Combating atherosclerosis with targeted nanomedicines: recent advances and future prospective.

Introduction: Cardiovascular diseases (CVDs) is recognized as the leading cause of mortality worldwide. The increasing prevalence of such disease demands novel therapeutic and diagnostic approaches to overcome associated clinical/social issues. Recent advances in nanotechnology and biological sciences have provided intriguing insights to employ targeted Nanomachines to the desired location as imaging, diagnosis, and therapeutic modalities. Nanomedicines as novel tools for enhanced drug delivery, imaging, and diagnosis strategies have shown great promise to combat cardiovascular diseases. Methods: In the current study, we intend to review the most recent studies on the nano-based strategies for improved management of CVDs. Results: A cascade of events results in the formation of atheromatous plaque and arterial stenosis. Furthermore, recent studies have shown that nanomedicines have displayed unique functionalities and provided de novo applications in the diagnosis and treatment of atherosclerosis. Conclusion: Despite some limitations, nanomedicines hold considerable potential in the prevention, diagnosis, and treatment of various ailments including atherosclerosis. Fewer side effects, amenable physicochemical properties and multi-potential application of such nano-systems are recognized through various investigations. Therefore, it is strongly believed that with targeted drug delivery to atherosclerotic lesions and plaque, management of onset and progression of disease would be more efficient than classical treatment modalities.