Reestablishment Of Blood Flow Research Articles

Network-Assisted Systems Biology Analysis of the Mitochondrial Proteome in a Pre-Clinical Model of Ischemia, Revascularization and Post-Conditioning.

Infarct size is the major risk predictor for developing heart failure after an acute myocardial infarction (AMI). The discovery of the conditioning phenomena (i.e., repetitive brief cycles of ischemia applied either before or after a prolonged ischemic insult) has highlighted the existence of endogenous protective mechanisms of the heart potentially limiting infarct size after revascularization. However, most cardioprotective strategies, aiming at infarct size reduction, have failed in clinical studies. Thus, cardioprotection is an unmet clinical need. In the present study, we took a network-assisted systems biology approach to explore the mitochondrial proteomic signature of the myocardium after ischemia, ischemia with direct revascularization, and ischemia with re-establishment of blood flow by post-conditioning in a swine model of AMI. Furthermore, network extension with the ENCODE project human regulatory data allowed the prediction of potential transcription factors at play in the response to post-conditioning of the myocardium. Collectively, our results identify cardiac metabolism as a driver of cardioprotection, highlighting a dual role for post-conditioning promoting metabolic reprogramming of the myocardium, and a protective response mediated by VDAC2 and DJ-1 in the mitochondria.

Breaking the fibrinolytic speed limit with microwheel co‐delivery of tissue plasminogen activator and plasminogen

BackgroundTo reestablish blood flow in vessels occluded by clots, tissue plasminogen activator (tPA) can be used; however, its efficacy is limited by transport to and into a clot and by the depletion of its substrate, plasminogen. ObjectivesTo overcome these rate limitations, a platform was designed to co‐deliver tPA and plasminogen based on microwheels (µwheels), wheel‐like assemblies of superparamagnetic colloidal beads that roll along surfaces at high speeds. MethodsThe biochemical speed limit was determined by measuring fibrinolysis of plasma clots at varying concentrations of tPA (10–800 nM) and plasminogen (1–6 µM). Biotinylated magnetic mesoporous silica nanoparticles were synthesized and bound to streptavidin‐coated superparamagnetic beads to make studded beads. Studded beads were loaded with plasminogen and tPA was immobilized on their surface. Plasminogen release and tPA activity were measured on the studded beads. Studded beads were assembled into µwheels with rotating magnetic fields and fibrinolysis of plasma clots was measured in a microfluidic device. ResultsThe biochemical speed limit for plasma clots was ~15 µm/min. Plasminogen‐loaded, tPA‐immobilized µwheels lyse plasma clots at rates comparableto the biochemical speed limit. With the addition of a corkscrew motion, µwheels penetrate clots, thereby exceeding the biochemical speed limit (~20 µm/min) and achieving lysis rates 40‐fold higher than 50 nM tPA. ConclusionsCo‐delivery of an immobilized enzyme and its substrate via a microbot capable of mechanical work has the potential to target and rapidly lyse clots that are inaccessible by mechanical thrombectomy devices or recalcitrant to systemic tPA delivery.

Abstract WP148: Magnetically Enhanced Diffusion (MED) Of Intravenous Thrombolytics Decreases Thrombus Leading To Accelerated Reperfusion

Whether systemic fibrinolysis alone or, more recently, combined with thrombectomy are used to re-establish blood flow in cerebral arteries occluded with thrombus, a shower of fragments often plugs more distal arterial branches leading to continued infarction, resulting in some loss of brain function. We hypothesized that magnetite MicroBeads injected intra-arterially near a thrombus and exposed to a rotating magnetic field after IV administration of plasminogen activators (lytics) would accelerate fibrinolysis leading to decreased distal thrombus burden, increased blood flow, and less brain infarction and loss of function. Clots formed in vitro from recalcified citrated rabbit blood were weighed (ave = 100mg) and injected into both common carotid arteries with blood flow occluded at the level of C3/4 in anesthetized male and female rabbits. rtPA (Activase, 1mg/kg, Genentech) was infused IV over 1h or Tenecteplase (TNK, 0.3-0.9mg/kg, Genentech) was injected IV as a bolus. After 30 min, magnetite MicroBeads were injected (300ug) as a bolus every 5 min over 30min (6 doses, 1,800mg) through a 5F angiocatheter placed within 2-3cm of the clot in one carotid, while the other carotid received the lytic alone by diffusion. The clots were removed after 1h and reweighed. MED increased the rate of fibrinolysis of clots leading to &gt95% reduction in clot weight vs 83% with Activase alone (p&lt0.0001 for paired testing, n=8). Clot lysis was also increased with MED + TNK (p&lt0.05, n=6) compared to TNK alone. Thus significant acceleration of lysis and reduction in clot weight occurs after treatment with MicroBeads plus lytic compared to lytic alone. This approach may enhance reperfusion and decrease infarction during stroke treated by either lytic alone or lytic + thrombectomy leading to improved outcomes.

Surgical treatment of a giant right coronary aneurysm following coronary stent fracture

Coronary artery aneurysm represents a challenging and potentially fatal disease. We present the case of a giant right coronary artery aneurysm treated surgically after percutaneous intervention and fracture of the stent. The aneurism was opened and the coronary ligated proximally and distally. It was not possible to re-established continuity of the coronary artery or perform a bypass graft. An early surgical strategy would have re-established blood flow in the involved coronary artery and avoided chronic ischemia of the supplied myocardial territory.

Short-duration hypothermia completed prior to reperfusion prevents intracranial pressure elevation following ischaemic stroke in rats

Reperfusion therapies re-establish blood flow after arterial occlusion and improve outcome for ischaemic stroke patients. Intracranial pressure (ICP) elevation occurs 18–24 h after experimental stroke. This elevation is prevented by short-duration hypothermia spanning the time of reperfusion. We aimed to determine whether hypothermia-rewarming completed prior to reperfusion, also prevents ICP elevation 24 h post-stroke. Transient middle cerebral artery occlusion was performed on male outbred Wistar rats. Sixty-minute hypothermia to 33 °C, followed by rewarming was induced prior to reperfusion in one group, and after reperfusion in another group. Normothermia controls received identical anaesthesia protocols. ΔICP from pre-stroke to 24 h post-stroke was measured, and infarct volumes were calculated. Rewarming pre-reperfusion prevented ICP elevation (ΔICP = 0.3 ± 3.9 mmHg vs. normothermia ΔICP = 5.2 ± 2.1 mmHg, p = 0.02) and reduced infarct volume (pre-reperfusion = 78.6 ± 23.7 mm3 vs. normothermia = 125.1 ± 44.3 mm3, p = 0.04) 24 h post-stroke. There were no significant differences in ΔICP or infarct volumes between hypothermia groups rewarmed pre- or post-reperfusion. Hypothermia during reperfusion is not necessary for prevention of ICP rise or infarct volume reduction. Short-duration hypothermia may be an applicable early treatment strategy for stroke patients prior to- during-, and after reperfusion therapy.

Urocortin Role in Ischemia Cardioprotection and the Adverse Cardiac Remodeling.

Despite the considerable progress in strategies of myocardial protection, ischemic heart diseases (IHD) and consequent heart failure (HF) remain the main cause of mortality worldwide. Several procedures are used routinely to guarantee the prompt and successful reestablishment of blood flow to preserve the myocardial viability of infarcted hearts from ischemia injuries. However, ischemic heart reperfusion/revascularization triggers additional damages that occur when oxygen-rich blood re-enters the vulnerable myocardial tissue, which is a phenomenon known as ischemia and reperfusion (I/R) syndrome. Complications of I/R injuries provoke the adverse cardiac remodeling, involving inflammation, mishandling of Ca2+ homeostasis, apoptotic genes activation, cardiac myocytes loss, etc., which often progress toward HF. Therefore, there is an urgent need to develop new cardioprotective therapies for IHD and HF. Compelling evidence from animal studies and pilot clinical trials in HF patients suggest that urocortin (Ucn) isoforms, which are peptides associated with stress and belonging to the corticotropin releasing factor family, have promising potential to improve cardiovascular functions by targeting many signaling pathways at different molecular levels. This review highlights the current knowledge on the role of urocortin isoforms in cardioprotection, focusing on its acute and long-term effects.

Novel Pharmacomechanical Thrombolysis for Treating Intermediate-Risk Acute Pulmonary Embolism: The Bashir Endovascular Catheter.

Novel Pharmacomechanical Thrombolysis for Treating Intermediate-Risk Acute Pulmonary Embolism: The Bashir Endovascular Catheter.

Remote but not Distant: a Review on Experimental Models and Clinical Trials in Remote Ischemic Conditioning as Potential Therapy in Ischemic Stroke.

Stroke is one of the main causes of neurological disability worldwide and the second cause of death in people over 65 years old, resulting in great economic and social burden. Ischemic stroke accounts for 85% of total cases, and the approved therapies are based on re-establishment of blood flow, and do not directly target brain parenchyma. Thus, novel therapies are urgently needed. In this review, limb remote ischemic conditioning (RIC) is revised and discussed as a potential therapy against ischemic stroke. The review targets both (i) fundamental research based on experimental models and (ii) clinical research based on clinical trials and human interventional studies with healthy volunteers. Moreover, it also presents two approaches concerning RIC mechanisms in stroke: (i) description of the underlying cerebral cellular and molecular mechanisms triggered by limb RIC that promote neuroprotection against stroke induced damage and (ii) the identification of signaling factors involved in inter-organ communication following RIC procedure. Limb to brain remote signaling can occur via circulating biochemical factors, immune cells, and/or stimulation of autonomic nervous system. In this review, these three hypotheses are explored in both humans and experimental models. Finally, the challenges involved in translating experimentally generated scientific knowledge to a clinical setting are also discussed.

Acute Ischemic Priapism: An AUA/SMSNA Guideline.

Priapism is a persistent penile erection that continues hours beyond, or is unrelated to, sexual stimulation and results in a prolonged and uncontrolled erection. Given its time-dependent and progressive nature, priapism is a situation that both urologists and emergency medicine practitioners must be familiar with and comfortable managing. Acute ischemic priapism, characterized by little or no cavernous blood flow and abnormal cavernous blood gases (ie, hypoxic, hypercarbic, acidotic) represents a medical emergency and may lead to cavernosal fibrosis and subsequent erectile dysfunction. A comprehensive search of the literature was performed by Emergency Care Research Institute for articles published between January 1, 1960 and May 1, 2020. Searches identified 2948 potentially relevant articles, and 2516 of these were excluded at the title or abstract level for not meeting inclusion criteria for any key question. Full texts for the remaining 432 articles were reviewed, and ultimately 137 unique articles were included in the report. This Guideline was developed to inform clinicians on the proper diagnosis and surgical and non-surgical treatment of patients with acute ischemic priapism. This Guideline addresses the role of imaging, adjunctive laboratory testing, early involvement of urologists when presenting to the emergency room, discussion of conservative therapies, enhanced data for patient counseling on risks of erectile dysfunction and surgical complications, specific recommendations on intracavernosal phenylephrine with or without irrigation, the inclusion of novel surgical techniques (eg, tunneling), and early penile prosthesis placement. All patients with priapism should be evaluated emergently to identify the sub-type of priapism (acute ischemic versus non-ischemic) and those with an acute ischemic event should be provided early intervention. Treatment of the acute ischemic patient must be based on patient objectives, available resources, and clinician experience. As such, a single pathway for managing the condition is oversimplified and no longer appropriate. Using a diversified approach, some men may be treated with intracavernosal injections of phenylephrine alone, others with aspiration/irrigation or distal shunting, and some may undergo non-emergent placement of a penile prosthesis.

Complex Syndrome of the Complete Occlusion of the End of the Superior Mesenteric Vein, Opposed with the Stable Gastric Pentadecapeptide BPC 157 in Rats.

Background. Gastric pentadecapeptide BPC 157 therapy in rats compensated irremovable occlusion of various vessels and counteracted the consequent multiorgan dysfunction syndromes by activation of the corresponding collateral bypassing loops. Thus, we used BPC 157 therapy against the irremovable occlusion of the end of the superior mesenteric vein. Methods. Assessments, for 30 min (gross recording, venography, ECG, pressure, microscopy, biochemistry, and oxidative stress) include the portal and caval hypertension, aortal hypotension, and centrally, the superior sagittal sinus hypertension, systemic arterial and venous thrombosis, ECG disturbances, MDA-tissue increase, and heart, lung, liver, kidney and gastrointestinal tract, in particular, and brain (cortex (cerebral, cerebellar), hypothalamus/thalamus, hippocampus) lesions. Rats received BPC 157 medication (10 µg/kg, 10 ng/kg) intraperitoneally at 1 or 15 min ligation time. Results. BPC 157 rapidly activated the superior mesenteric vein–inferior anterior pancreati-coduodenal vein–superior anterior pancreaticoduodenal vein–pyloric vein–portal vein pathway, reestablished superior mesenteric vein and portal vein connection and reestablished blood flow. Simultaneously, toward inferior caval vein, an additional pathway appears via the inferior mesenteric vein united with the middle colic vein, throughout its left colic branch to ascertain alternative bypassing blood flow. Consequently, BPC 157 acts peripherally and centrally, and counteracted the intracranial (superior sagittal sinus), portal and caval hypertension, aortal hypotension, ECG disturbances attenuated, abolished progressing venous and arterial thrombosis. Additionally, BPC 157 counteracted multiorgan dysfunction syndrome, heart, lung, liver, kidney and gastrointestinal tract, and brain lesions, and oxidative stress in tissues. Conclusion. BPC 157 therapy may be specific management also for the superior mesenteric vein injuries.

Cellular crosstalk in cardioprotection: Where and when do reactive oxygen species play a role?

A well-balanced intercellular communication between the different cells within the heart is vital for the maintenance of cardiac homeostasis and function. Despite remarkable advances on disease management and treatment, acute myocardial infarction remains the major cause of morbidity and mortality worldwide. Gold standard reperfusion strategies, namely primary percutaneous coronary intervention, are crucial to preserve heart function. However, reestablishment of blood flow and oxygen levels to the infarcted area are also associated with an accumulation of reactive oxygen species (ROS), leading to oxidative damage and cardiomyocyte death, a phenomenon termed myocardial reperfusion injury. In addition, ROS signaling has been demonstrated to regulate multiple biological pathways, including cell differentiation and intercellular communication. Given the importance of cell-cell crosstalk in the coordinated response after cell injury, in this review, we will discuss the impact of ROS in the different forms of inter- and intracellular communication, as well as the role of gap junctions, tunneling nanotubes and extracellular vesicles in the propagation of oxidative damage in cardiac diseases, particularly in the context of ischemia/reperfusion injury.

Method of intra-arterial drug administration in a rat: Sex based optimization of infusion rate

BackgroundEndovascular thrombectomy is the process of removing a blood clot and re-establishing blood flow in patients with emergent large vessel occlusion. The technique provides an opportunity to deliver therapeutics directly to the site of injury. The intra-arterial (IA) route of drug administration in the mouse was developed to bridge the gap between animal stroke treatments and clinical stroke therapy. Here, we adapted the IA method for use in rats, by investigating various flow rates to optimize the IA injection through the internal carotid artery (ICA). MethodsMale and female Sprague-Dawley rats (∼4 months of age) were subjected to placement of micro-angio tubing at the bifurcation of the common carotid artery for injection into the ICA. We evaluated a range of infusion rates of carbon black ink and its vascular distribution within the brain. ResultsOptimal injection rates in males was 4−6 μl/min and 2−4 μl/min in females. The IA injection using these sex-specific rates resulted in appropriate limited dye delivery to only the ipsilateral region of the brain, without inducing a subarachnoid hemorrhage. ConclusionUpon adapting the IA administration model to rats, it was determined that the rate of infusion varied between males and females. This variability is an important consideration for studies utilizing both sexes, such as in ischemic stroke studies.

HSPA12B Expression as an Epigenetic Signature Following Ischemic Stroke: Heat Shock Protein Mini Review

Stroke is a cardiovascular condition that caused by a clot or obstruction that prevents blood from flowing to the brain. Neural cells within the occluded area undergo cell death within minutes, and the results are often permanent, making stroke one of the leading causes of serious longterm disability. Stroke is a complex disorder that requires innovative solutions to attenuate the effects of stroke and improve clinical outcomes. Traditionally, stroke treated by relieving vascular occlusions and restoring blood flow to the infarcted tissue (necrotic tissue; core infarct) and the surrounding tissue at risk (penumbra). This technique known as thrombolysis, utilizing both chemical and mechanical modes. Chemical thrombolysis utilizes a catheter that administers medication to the clot site, which includes a multitude of treatments that include intravenous (IV) thrombolysis with recombinant tissue plasminogen activator, or rTPA, and intra-arterial (IA) therapies that aim to directly remove the occlusive clot and reestablish blood flow through recanalization.

Anterior Spinal Artery Syndrome due to Intervertebral Disc Herniation: A Systematic Review

Objective: Anterior spinal artery syndrome (ASAS) has been rarely reported as a complication of intervertebral disc herniation (IVDH). Precipitation factors, presentation, evaluation, treatment strategy, and degrees of recovery have not yet been well documented. Methods: Systematic review was conducted according to PRISMA guidelines to review and summarize for the qualitative synthesis of the data from reported cases of anterior spinal artery syndrome due to intervertebral disc herniation from 1980 to February 2021. Results: A total of 12 cases were reviewed, the median age was 48.5 years. Motor weakness with or without pain was the most frequent presenting symptom accompanying bowel or bladder incontinence (25%) or diminished pain and temperature sensation with spared dorsal column sensation. 40% of conservatively treated patients had complete recovery without any residual deficit. Whereas all patients who managed surgically regained fully functional status with shorter recovery intervals. Conclusion: Abrupt onset of motor weakness is a potential warning symptom of spinal cord infarction, rarely attributed to ASA compression by a herniated disc. Moreover, an accompanying diminished pain and temperature sensation with spared dorsal column sensation is further intimation. Reestablishment of blood flow may bear a favorable outcome.

Iatrogenic Left Main Coronary Artery Dissection Treated with Bare Metal Stents: A Case with Twelve Years Angiographic Follow-up

Complications during the course of Percutaneous Coronary Interventions (PCI) are common. One of the complications is iatrogenic Left Main Coronary Artery (LMCA) dissection, which is considered as lethal in nature and prevails in around 0.07% PCI cases. Timely diagnosis and immediate revascularisation is mandatory to manage LMCA dissection in order to avoid worsening of patient’s haemodynamic condition and to re-establish antegrade coronary blood flow. Here, the author report a case of catheter-induced iatrogenic LMCA dissection developed during stenting of a lesion in Left Anterior Descending (LAD) coronary artery of a 32-year-old male patient. The patient was managed by implantation of two Matrix (Sahajanand Medical Technologies, Pvt., Ltd., Surat, India) Bare Metal Stents (BMS) using double barrel technique to treat the dissection in left main coronary bifurcation. The patient was regularly followed-up and even after 12 years of the index procedure, the angiographic data revealed good patency of stents in LMCA without any major cardiac events.

Iatrogenic Left Main Coronary Artery Dissection Treated with Bare Metal Stents: A Case with Twelve Years Angiographic Follow-up

Complications during the course of Percutaneous Coronary Interventions (PCI) are common. One of the complications is iatrogenic Left Main Coronary Artery (LMCA) dissection, which is considered as lethal in nature and prevails in around 0.07% PCI cases. Timely diagnosis and immediate revascularisation is mandatory to manage LMCA dissection in order to avoid worsening of patient’s haemodynamic condition and to re-establish antegrade coronary blood flow. Here, authors report a case of catheter-induced iatrogenic LMCA dissection developed during stenting of a lesion in Left Anterior Descending (LAD) coronary artery of a 32-year-old male patient. The patient was managed by implantation of two Matrix (Sahajanand Medical Technologies, Pvt., Ltd., Surat, India) Bare Metal Stents (BMS) using double barrel technique to treat the dissection in left main coronary bifurcation. The patient was regularly followed-up and even after 12 years of the index procedure, the angiographic data revealed good patency of stents in LMCA without any major cardiac events.

Iatrogenic Left Main Coronary Artery Dissection Treated with Bare Metal Stents: A Case with Twelve Years Angiographic Follow-up

Complications during the course of Percutaneous Coronary Interventions (PCI) are common. One of the complications is iatrogenic Left Main Coronary Artery (LMCA) dissection, which is considered as lethal in nature and prevails in around 0.07% PCI cases. Timely diagnosis and immediate revascularisation is mandatory to manage LMCA dissection in order to avoid worsening of patient’s haemodynamic condition and to re-establish antegrade coronary blood flow. Here, authors report a case of catheter-induced iatrogenic LMCA dissection developed during stenting of a lesion in Left Anterior Descending (LAD) coronary artery of a 32-year-old male patient. The patient was managed by implantation of two Matrix (Sahajanand Medical Technologies, Pvt., Ltd., Surat, India) Bare Metal Stents (BMS) using double barrel technique to treat the dissection in left main coronary bifurcation. The patient was regularly followed-up and even after 12 years of the index procedure, the angiographic data revealed good patency of stents in LMCA without any major cardiac events.

Skeletal Muscle Mitochondrial Dysfunction and Oxidative Stress in Peripheral Arterial Disease: A Unifying Mechanism and Therapeutic Target.

Peripheral artery disease (PAD) is caused by atherosclerosis in the lower extremities, which leads to a spectrum of life-altering symptomatology, including claudication, ischemic rest pain, and gangrene requiring limb amputation. Current treatments for PAD are focused primarily on re-establishing blood flow to the ischemic tissue, implying that blood flow is the decisive factor that determines whether or not the tissue survives. Unfortunately, failure rates of endovascular and revascularization procedures remain unacceptably high and numerous cell- and gene-based vascular therapies have failed to demonstrate efficacy in clinical trials. The low success of vascular-focused therapies implies that non-vascular tissues, such as skeletal muscle and oxidative stress, may substantially contribute to PAD pathobiology. Clues toward the importance of skeletal muscle in PAD pathobiology stem from clinical observations that muscle function is a strong predictor of mortality. Mitochondrial impairments in muscle have been documented in PAD patients, although its potential role in clinical pathology is incompletely understood. In this review, we discuss the underlying mechanisms causing mitochondrial dysfunction in ischemic skeletal muscle, including causal evidence in rodent studies, and highlight emerging mitochondrial-targeted therapies that have potential to improve PAD outcomes. Particularly, we will analyze literature data on reactive oxygen species production and potential counteracting endogenous and exogenous antioxidants.

Damage-Associated Molecular Patterns in Myocardial Infarction and Heart Transplantation: The Road to Translational Success.

In the setting of myocardial infarction (MI), ischemia reperfusion injury (IRI) occurs due to occlusion (ischemia) and subsequent re-establishment of blood flow (reperfusion) of a coronary artery. A similar phenomenon is observed in heart transplantation (HTx) when, after cold storage, the donor heart is connected to the recipient’s circulation. Although reperfusion is essential for the survival of cardiomyocytes, it paradoxically leads to additional myocardial damage in experimental MI and HTx models. Damage (or danger)-associated molecular patterns (DAMPs) are endogenous molecules released after cellular damage or stress such as myocardial IRI. DAMPs activate pattern recognition receptors (PRRs), and set in motion a complex signaling cascade resulting in the release of cytokines and a profound inflammatory reaction. This inflammatory response is thought to function as a double-edged sword. Although it enables removal of cell debris and promotes wound healing, DAMP mediated signalling can also exacerbate the inflammatory state in a disproportional matter, thereby leading to additional tissue damage. Upon MI, this leads to expansion of the infarcted area and deterioration of cardiac function in preclinical models. Eventually this culminates in adverse myocardial remodeling; a process that leads to increased myocardial fibrosis, gradual further loss of cardiomyocytes, left ventricular dilation and heart failure. Upon HTx, DAMPs aggravate ischemic damage, which results in more pronounced reperfusion injury that impacts cardiac function and increases the occurrence of primary graft dysfunction and graft rejection via cytokine release, cardiac edema, enhanced myocardial/endothelial damage and allograft fibrosis. Therapies targeting DAMPs or PRRs have predominantly been investigated in experimental models and are potentially cardioprotective. To date, however, none of these interventions have reached the clinical arena. In this review we summarize the current evidence of involvement of DAMPs and PRRs in the inflammatory response after MI and HTx. Furthermore, we will discuss various current therapeutic approaches targeting this complex interplay and provide possible reasons why clinical translation still fails.

The effect of heparin after primary percutaneous coronary intervention on short-term clinical outcomes in patients with ST-segment elevation myocardial infarction

Background: Doing percutaneous coronary intervention (PCI) in the first hours of myocardial infraction (MI) is effective in re-establishment of blood flow. Anticoagulation treatment should be prescribed in patients undergoing PCI to decrease the side effects of ischemia. The aim of this study is to determine the effect of heparin prescription after PCI on short-term clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI). Materials: This randomized clinical trial study was conducted at Imam Ali cardiovascular center at Kermanshah university of medical science (KUMS), Iran. Between April 2019 to October 2019, 400 patients with STEMI which candidate to PCI were enrolled. Patients randomly divided in two groups: intervention group (received 5,000 units of heparin after PCI until first 24 hours, every 6 hours) and control group (did not receive heparin). Data were collected using a checklist developed based on the study's aims. Differences between groups were assessed using independent t-tests and chi-square (or Fisher exact tests).Result: Observed that, mean prothrombin time (PT) (13.30±1.60 vs. 12.21±1.15, p<0.001) and partial thromboplastin time (PTT) (35.30±3.08 vs. 34.41±3.01, p=0.003) were significantly higher in intervention group compared to control group. Thrombolysis in myocardial infarction (TIMI) flow grade 0/1 after primary PCI was significantly more frequently in control group (5.5% vs. 1.0%, p=0.034). The mean of ejection fraction (EF) after PCI (47.58±7.12 vs. 45.15±6.98, p<0.001) was significantly higher in intervention group. Intervention group had a statistically significant shorter length of hospital stay (4.71±1.03 vs. 6.12±1.10, p<0.001). There was higher incidence of re-vascularization (0% vs. 3.0%; p=0.013) and re-MI (0% vs. 2.5%; p=0.024) in the control group.Conclusion: Performing primary PCI with receiving heparin led to improve TIMI flow and consequently better EF. Receiving heparin is associated with lower risk of re-MI and re-vascularization.