Inadequate Myocardial Perfusion Research Articles

Coronary No-Reflow after Primary Percutaneous Coronary Intervention

Coronary no-reflow is a significant complication following primary percutaneous coronary intervention (PCI) in patients with acute myocardial infarction. This phenomenon involves inadequate myocardial perfusion despite successful vessel recanalization, attributed to factors such as microvascular injury, inflammation, thrombus embolization, and vasospasm. Effective management strategies include pharmacological agents, mechanical interventions, and optimized antithrombotic therapy. Prompt diagnosis and treatment are essential to enhance patient outcomes and reduce adverse effects associated with this condition.

Practical Approach to Diagnosis, Prevention, and Management of Coronary No-Reflow

Coronary no-reflow (NR) defined as inadequate myocardial perfusion despite restoration of coronary artery patency is a bane for an interventional cardiologist. It can complicate percutaneous coronary interventions especially in the setting of STEMI and dampens the potential benefits of PPCI. Broadly classified as Reperfusion NR and Interventional NR, mechanism is multifactorial. The basic underlying culprit is microvascular obstruction either secondary to distal embolization, intravascular plugging, or ischemic reperfusion injury. Coronary angiogram is an easy, readily available, and essential modality to diagnose no-reflow, but the gold standard is gadolinium-enhanced cardiovascular magnetic resonance imaging. Preventive strategies for NR should be integral part of prePCI planning especially in clinical scenario where NR is expected such as STEMI with delayed presentation and high thrombus burden, atherectomy, and SVG PCI. The cornerstone of treatment for NR is local vasodilators and antiplatelet therapy to ameliorate vasospasm and thromboembolism respectively, and different combinations of the two should be used in no specific order to achieve reversal of NR. NR phenomenon is associated with poor short-term and long-term prognosis and every attempt should be made to avoid or reverse it. Therapeutic hypothermia, hyperoxemic reperfusion therapy, targeted anti-inflammatory approach, and cellular approach appear proising but further research is mandatory.

Prognostication of left ventricular remodeling in obese patients with ST-segment elevation myocardial infarction

Background and Aims : The high level of adipose tissue promotes inadequate myocardial perfusion and following this pathologic cardiac remodeling and heart failure in future. Thus, to determine predictors of pathological remodeling in patients with ST-segment elevation myocardial infarction (STEMI) with obesity is very significant.

Impact of intracoronary reteplase during primary percutaneous coronary intervention on infarct size in large anterior myocardial infarction: rationale and design of the RECOVER II trial

Thrombus embolization and microvascular obstruction during percutaneous coronary intervention (PCI) in ST-segment elevation myocardial infarction (STEMI) is commonly detected, which causes inadequate myocardial perfusion and elevated infarct size. An approach with low-dose intracoronary fibrinolytic treatment for reducing distal embolization and improving myocardial reperfusion in high-risk STEMI cases remains controversial. The RECOVER II study represents a multicenter, randomized, double-blind, parallel-group trial assessing low-dose adjunctive intracoronary reteplase during primary PCI in individuals with large anterior myocardial infarction and thrombus determined by angiography. The trial will enroll 306 cases who present within 12 h following STEMI for proximal or mid left anterior descending artery occlusion undergoing primary PCI. Cases will be randomized to receive a bolus intracoronary reteplase at 9 mg or 18 mg vs. placebo. The drug will be delivered over 2 minutes proximal to culprit lesions with an intracoronary catheter early after wire-crossing and before thrombus aspiration or balloon dilation. The primary outcome will be infarct size assessed by late gadolinium-enhanced magnetic resonance imaging (MRI) (% of left ventricular mass) on day 7 after enrollment. Secondary outcomes will include the amount of microvascular obstruction and myocardial salvage index examined via MRI on day 7, angiographic measures of reperfusion [Thrombolysis in Myocardial Infarction (TIMI) coronary flow grade, TIMI frames count and myocardial blush grade], incidence of complete ST-segment resolution at 2 hours after reperfusion, area under the curve for troponin T, and rates of major adverse cardiovascular events at 30 days. RECOVER II will determine whether the addition of low-dose intracoronary reteplase early after wire-crossing as an adjunct to reperfusion treatment reduces infarct size in individuals with large anterior myocardial infarction. ClinicalTrials.gov Identifier: NCT04571580.

"No-Reflow" Phenomenon: A Contemporary Review.

Primary percutaneous angioplasty (pPCI), represents the reperfusion strategy of choice for patients with STEMI according to current international guidelines of the European Society of Cardiology. Coronary no-reflow is characterized by angiographic evidence of slow or no anterograde epicardial flow, resulting in inadequate myocardial perfusion in the absence of evidence of mechanical vessel obstruction. No reflow (NR) is related to a functional and structural alteration of the coronary microcirculation and we can list four main pathophysiological mechanisms: distal atherothrombotic embolization, ischemic damage, reperfusion injury, and individual susceptibility to microvascular damage. This review will provide a contemporary overview of the pathogenesis, diagnosis, and treatment of NR.

Abstract 10644: Impact of Cardiopulmonary Bypass Surgery on Myocardial Perfusion Assessed by Ultrafast Power Doppler: A Human Proof-of-Concept Study

Introduction: Inadequate myocardial coronary perfusion is a major cause of cardiac dysfunction in several clinical settings including congenital heart disease and cardiopulmonary bypass surgery (CPB). Blood flow to the myocardium (i.e. coronary perfusion) is primarily controlled by the coronary microvasculature (vessels < 500 μm) which plays a key part in coronary perfusion autoregulation. Until recently, direct quantitative coronary perfusion assessment had been infeasible due to limitations in spatial and/or temporal resolution of clinical imaging modalities. The study objective is to assess if ultrafast ultrasound-mediated power Doppler (PD) can approximate changes in myocardial perfusion in humans. Methods: We used a 6.9 MHz linear array probe connected to a programmable ultrafast ultrasound scanner (Verasonics Vantage®). We included 7 neonates with transposition of the great arteries (TGA) and acquired epicardial ultrafast acquisitions immediately before and after CPB (arterial switch operation) via open chest. The acquisitions were acquired at 2000 fps (PRF=10000Hz, 5 sources). Tissue clutter was separated from coronary signals with a sliding spatiotemporal filter. PD was measured as a representative of blood volume that scales with hematocrit. Fractional moving blood volume (FMBV) was calculated to normalize the PD signal: mean PD divided by the PD of the ventricular blood pool, a region with 100% vascular amplitude. Results and Conclusions: The FMBV post-operatively increased by a factor of two compared to pre-operative assessment, a reflection of hyperemia. These values returned to baseline on repeat assessment prior to discharge. Our findings suggest that ultrafast PD is a reliable tool in approximating changes in myocardial perfusion in the operating room and beyond. Thus, ultrafast power Doppler can be utilized to quantitatively assess the impact of CPB on coronary perfusion in humans.

Manifestation of Acute Coronary Syndrome in Critically Aortic Stenosis Patients

The clinical presentation of acute coronary syndromes (ACS) is broad, from cardiac arrest, electrical or haemodynamic instability with cardiogenic shock (CS) due to ongoing ischaemia or mechanical complications such as severe mitral regurgitation, to patients who are already pain free again at the time of presentation. Critical aortic stenosis (AS) can cause inadequate myocardial perfusion and in the absence of demonstrable coronary stenosis or occlusion which resulting in ACS manifestation. Critical AS (defined as valve area <0.5 cm2) has been reported to cause mild increases in cardiac biomarkers such as troponin I. A 56-year-old man was admitted to hospital with chief complaint of typcal chest pain. Electrocardiogram (ECG) shows myocardial infarction in left main (LM) equivalent. Echocardiography revealed critical aortic stenosis. Cardiac marker also shows increasing. However, diagnostic coronary angiography (DCA) did not identify any lesions to account for the patient’s electrocardiographic changes and ongoing symptoms of chest pain. Consultation to cardiothorax surgeon to have urgent aortic valve replacement (AVR) were planned and underwent successful aortic valve (AV) replacement without coronary intervention. The definitive treatment for symptomatic severe AS is AVR. Some of the treatments that can be done are immediate coronary angiography and reperfusion procedure if there is suspicion of coronary artery occlusion or stenosis which may cause myocardial infarction; Intra-Aortic Ballon Pump (IABP) if there are signs of myocardial injury with take caution to the contraindications of IABP placement; Perform intervention procedure as soon as possible on aortic valve; Administration of medical therapy for heart failure in symptomatic severe AS patients. The case emphasizes the importance of initial physical examination, ECG, echocardiography, and cardiac markers as a whole that we do in aortic valve stenosis patient presenting with ACS.

State of the Art: No-Reflow Phenomenon.

Primary percutaneous coronary intervention is the preferred reperfusion strategy for the management of acute ST-segment elevation myocardial infarction. No reflow is characterized by the inadequate myocardial perfusion of a given segment without angiographic evidence of persistent mechanical obstruction of epicardial vessels. Both pharmacologic and device-based strategies have been tested to resolve coronary no reflow. This article provides an updated overview of the no-reflow phenomenon, discussing clinical evidence and ongoing investigations of existing and novel therapeutic strategies to counteract it.

Microvasculature Recovery by Angiogenesis After Myocardial Infarction

Advances in early reperfusion therapies focused on the revascularization of the ischemic tissues, in the last decades, lead to reduced mortality in acute myocardial infarction (MI) patients. However, a large proportion of patients show inadequate myocardial perfusion because of dysfunction of the microcirculation. The high prevalence of microvascular dysfunction after reperfusion therapies and the negative prognostic of this procedure justify the search for therapeutic strategies that aim to restore the microvascular network. It is well known that the size of the initial infarct, the duration of ischemia and the efficiency of reperfusion determine myocardial tissue damage and cardiomyocyte loss after myocardial infarction. Therefore any advancement on the mechanisms that induce the repair process of microvascular dysfunction after reperfused MI is of great interest. Here, we will review the different proteins and cells known to participate in angiogenesis induction post-MI and we will also discuss the potential pharmacological and cellular processes that promote the recovery of microvasculature by angiogenesis stimulation after MI.

Abstract 455: Role of Transcription Co-Factor Friend of GATA 2 (FOG2) in a Hypertensive-Diabetic Mouse Model of Coronary Microvascular Disease

Coronary microvascular disease (CMVD) - disease of the coronary pre-arterioles, arterioles, and capillaries – has become an increasingly well-recognized cardiac pathology. Characterized by microvascular remodeling, wall thickening, lumen obliteration, endothelial dysfunction, capillary rarefaction, and perivascular immune cell infiltration, it can lead to inadequate myocardial perfusion, angina, heart failure, or myocardial infarction. Despite these clinical ramifications, our understanding of the pathophysiology of CMVD remains nascent. Friend of GATA 2 (FOG2, also called ZFPM2) is a transcriptional co-factor which is crucial in coronary development; and cardiomyocyte expression of FOG2 is required for the maintenance of the coronary microvasculature in adult mice. We hypothesize that FOG2 is activated in CMVD, and that Hypoxia-Inducible Factor 1a (HIF1a) may play a role in FOG2 activation. To test this hypothesis, we developed a hypertensive-diabetic (HTN/DM) mouse model of CMVD. Briefly, adult female C57BL/6 mice were treated with Angiotensin II (1mg/kg/day SQ osmotic pump for 8 weeks) and low-dose streptozotocin (35 mg/kg IP for 4 days) (n=5) or saline (n=4). HTN/DM mice had increased systolic blood pressure (141.7±1.6 vs 109.2±1.1 mmHg, p<0.0001), mild fasting hyperglycemia (181.8±8.5 vs 148.8±9.8 mg/dl, p=0.04), and decreased glucose tolerance (p<0.0003). HTN/DM mice had evidence of mild LV hypertrophy, preserved EF, and diminished coronary hyperemic velocities by echocardiography. Histology revealed microvascular pathology (vessel wall thickening and immune cell infiltration) and decreased cardiac capillary density (148.8±9.8 vs 163.8±4.3 phf, p=0.008). FOG2 protein was increased in HTN/DM mouse hearts (p<0.05). Treatment of AC16 cardiomyocytes with HIF-activator hydroxylase inhibitor DMOG showed a dose-dependent increase in FOG2 expression and protein nuclear translocation. In summary, we modeled CMVD in mice using mild hypertensive-diabetic insults which are relevant to human disease. We found that FOG2 protein is increased in CMVD suggesting that FOG2 may be relevant to adult CMVD pathophysiology in vivo . We additionally provide in vitro evidence that FOG2 is induced in HIF-activating conditions .

Abstract 219: Role of Transcription Co-Factor Friend of GATA 2 (FOG2) in a Hypertensive-Diabetic Mouse Model of Coronary Microvascular Disease

Coronary microvascular disease (CMVD), or disease of the coronary pre-arterioles, arterioles, and capillaries, has become an increasingly well-recognized cardiac pathology. Characterized by microvascular remodeling, wall thickening, lumen obliteration, endothelial dysfunction, capillary rarefaction, and perivascular immune cell infiltration, CMVD can lead to inadequate myocardial perfusion, angina, heart failure, or myocardial infarction. Despite significant clinical ramifications, our understanding of the pathophysiology of CMVD remains nascent. Friend of GATA 2 (FOG2, also ZFPM2) is a crucial transcriptional co-factor in coronary development; and cardiomyocyte expression of FOG2 is required for the maintenance of the coronary microvasculature in adult mice. We hypothesize that FOG2 is activated in CMVD, and that Hypoxia-Inducible Factor 1a (HIF1a) may play a role in FOG2 activation. To test this hypothesis, we developed a hypertensive-diabetic (HTN/DM) mouse model of CMVD. Briefly, adult female C57BL/6 mice were treated with Angiotensin II (1mg/kg/day osmotic pump for 8 weeks) and low-dose streptozotocin (35 mg/kg IP for 4 days) (n=5) or saline (n=4). HTN/DM mice had increased systolic blood pressure (142±2 mmHg v 109±1 mmHg, p<1e4), mild fasting hyperglycemia (182±9 mg/dl v 149±10 mg/dl, p=0.04), and decreased glucose tolerance (p<3e4). These resulted in decreased cardiac capillary density (149±10 v 164±4 phf, p=0.008) and evidence of microvascular pathology including vessel wall thickening and immune cell infiltration. HTN/DM mice had mild LV hypertrophy, preserved EF, and diminished coronary hyperemic velocities by echocardiography. Cardiac FOG2 protein was increased in HTN/DM mice (p<0.05). To examine the relationship between HIF and FOG2 in vitro , AC16 cardiomyocytes were treated with HIF-hydroxylase inhibitor DMOG (0.1mM, 1mM) for 16 hours. There was a dose-dependent increase in FOG2 expression and nuclear translocation. In summary, we developed a mouse model of CMVD with mild hypertensive-diabetic insults which are relevant to human disease. We found that FOG2 protein is increased in CMVD suggesting that FOG2 may be relevant to adult CMVD pathophysiology in vivo . We additionally provide in vitro evidence that FOG2 is induced in HIF-activating conditions.

Neutrophil/Lymphocyte Ratio as a Predictor of In-Hospital Major Adverse Cardiac Events, New-Onset Atrial Fibrillation, and No-Reflow Phenomenon in Patients with ST Elevation Myocardial Infarction.

BACKGROUNDNeutrophil/lymphocyte (N/L) ratio represents the balance between neutrophil and lymphocyte counts in the body and can be utilized as an index for systemic inflammatory status. The no-reflow phenomenon is defined as inadequate myocardial perfusion through a given segment of the coronary circulation without angiographic evidence of mechanical vessel obstruction. Systemic inflammatory status has been associated with new-onset atrial fibrillation (NOAF) as well as no-reflow.AIMTo evaluate the predictive value of N/L ratio for in-hospital major adverse events, NOAF, and no-reflow in patients with ST elevation myocardial infarction (STEMI).PATIENTSTwo hundred consecutive patients with STEMI presenting to Alexandria Main University Hospital and International Cardiac Center Hospital, Alexandria, Egypt, from April 2013 to October 2013 were included in this study.METHODSLaboratory investigation upon admission included complete blood count with mean platelet volume (MPV) and N/L ratio, and random plasma glucose (RPG) level. The results of coronary angiography indicating the infarct-related artery (IRA), initial thrombolysis in myocardial infarction (TIMI) flow in the IRA, and the TIMI flow after stenting were recorded. The patients were studied according to the presence of various clinical and laboratory variables, such as age, gender, pain-to-balloon time, location of the infarction, RPG level and complete blood count including N/L ratio and MPV on admission, and initial TIMI flow in the IRA. They were also evaluated for the final TIMI flow after the primary percutaneous coronary intervention, incidence of NOAF, and the incidence of in-hospital major adverse cardiac events (MACE).RESULTSThe incidence rate of no-reflow, NOAF, and in-hospital MACE was 13.2%, 8%, and 5%, respectively, with cardiac death as the predominant form of in-hospital MACE. The group of no-reflow, NOAF, and/or MACE showed significantly older age (62.29 ± 7.90 vs 56.30 ± 10.34, P = 0.014), longer pain-to-balloon time (15.90 ± 7.87 vs 6.08 ± 3.82 hours, P < 0.001), higher levels of RPG, N/L ratio (8.19 ± 3.05 vs 5.44 ± 3.53, P, 0.001), and MPV (11.90 ± 2.09 vs 8.58 ± 1.84 fL, P < 0.001) on admission. After adjustment of confounding factors, the independent predictors of NOAF, no-reflow, and in-hospital MACE were higher N/L ratio (odds ratio [OR] = 3.5, P = 0.02) and older age (OR = 3.1, P = 0.04).CONCLUSIONSOlder patient age, longer pain-to-balloon time, hyperglycemia, higher N/L ratio, and MPV on admission are useful predictive factors for the occurrence of no-reflow postprimary percutaneous coronary intervention, NOAF, and/or in-hospital MACE. N/L ratio is a new strong independent predictor of no-reflow, NOAF, and/or in-hospital MACE in patients with STEMI. The use of this simple routine biomarker may have a potential therapeutic implication in preventing NOAF and improving prognosis in STEMI revascularized patients.

Reduction of no-reflow and reperfusion injury with the synthetic 17β-aminoestrogen compound Prolame is associated with PI3K/Akt/eNOS signaling cascade.

A high proportion of primary percutaneous coronary interventions performed in the setting of acute myocardial infarction, concur with inadequate myocardial perfusion at the microvascular level. This phenomenon, known as "no-reflow" contributes to reperfusion injury, poor prognosis and to unfavorable clinical outcome. In this study, we evaluated the hypothesis that the synthetic 17β-aminoestrogen Prolame, may confer cardioprotection and prevent against no-reflow. In an open-chest model of 30-min ischemia and 90-min reperfusion, male Wistar rats were randomly assigned to different groups: Control, Prolame, Prolame followed by the nitric oxide synthase inhibitor (L-NAME), and 17β-estradiol. Areas of risk, infarct size and no-reflow were determined by planimetry with triphenyltetrazolium chloride and thioflavin-S stains. Structural damage of the vasculature was measured as capillary compression in clarified tissue after intra-atrial injection of Microfil. Hemodynamic function was obtained at the end of stabilization, ischemia and reperfusion; nitric oxide (NO·) content was determined indirectly using the Griess reaction. Activation of the eNOS signaling cascade was determined by western blot. Prolame reduced the infarcted area, decreased the zones of no-reflow and capillary compression by activating the PI3K/Akt/eNOS signaling pathway in correlation with NO· increase. Prolame also activated endothelial cells augmenting NO· production, which was inhibited by ICI182780 (a selective estrogen receptor down-regulator), supporting the notion that the cardioprotective effect of Prolame involves the preservation of endothelium through the activation of estrogen receptor downstream signaling. Our results provide evidence that Prolame has potential therapeutic application in patients with AMI, as it prevents from both vascular and cardiac tissue damage.

Obesity and coronary microvascular disease - implications for adipose tissue-mediated remote inflammatory response.

It is believed that obesity has detrimental effects on the coronary circulation. These include immediate changes in coronary arterial vasomotor responsiveness and the development of occlusive large coronary artery disease. Despite its critical role in regulating myocardial perfusion, the altered behavior of coronary resistance arteries, which gives rise to coronary microvascular disease (CMD) is poorly understood in obesity. A chronic, low-grade vascular inflammation has been long considered as one of the main underlying pathology behind CMD. The expanded adipose tissue and the infiltrating macrophages are the major sources of pro-inflammatory mediators that have been implicated in causing inadequate myocardial perfusion and, in a long term, development of heart failure in obese patients. Much less is known the mechanisms regulating the release of these cytokines into the circulation that enable them to exert their remote effects in the coronary microcirculation. This mini review aims to examine recent studies describing alterations in the vasomotor function of coronary resistance arteries and the role of adipose tissue-derived pro-inflammatory cytokines and adipokines in contributing to CMD in obesity. We provide examples of regulatory mechanisms by which adipokines are released from adipose tissue to exert their remote inflammatory effects on coronary microvessels. We identify some of the important challenges and opportunities going forward.

Protection of coronary endothelial function during cardiac surgery: potential of targeting endothelial ion channels in cardioprotection.

Vascular endothelium plays a critical role in the control of blood flow by producing vasoactive factors to regulate vascular tone. Ion channels, in particular, K+ channels and Ca2+-permeable channels in endothelial cells, are essential to the production and function of endothelium-derived vasoactive factors. Impairment of coronary endothelial function occurs in open heart surgery that may result in reduction of coronary blood flow and thus in an inadequate myocardial perfusion. Hyperkalemic exposure and concurrent ischemia-reperfusion during cardioplegic intervention compromise NO and EDHF-mediated function and the impairment involves alterations of K+ channels, that is, KATP and KCa, and Ca2+-permeable TRP channels in endothelial cells. Pharmacological modulation of these channels during ischemia-reperfusion and hyperkalemic exposure show promising results on the preservation of NO and EDHF-mediated endothelial function, which suggests the potential of targeting endothelial K+ and TRP channels for myocardial protection during cardiac surgery.

Modulation of Individual Susceptibility to the No-Reflow Phenomenon after Acute Myocardial Infarction

Coronary reperfusion using primary percutaneous coronary intervention (PCI) dramatically reduces morbidity and mortality among patients with acute myocardial infarction (AMI). Nevertheless, inadequate myocardial perfusion, known as the "no-reflow" phenomenon, is observed in approximately 15% of patients and is associated with poor outcomes. No-reflow is caused not only by mechanical occlusion of the microvasculature due to thromboembolism but also by myocardial injury. Transmural myocardial damage before PCI and the size of the associated area are major factors in the development of no-reflow. There is evidence indicating that inflammation, oxidative injury, morphological changes of endothelial cells, hyperglycemia, and absence of ischemic preconditioning also contribute to the development of no-reflow. Several strategies have been attempted to counteract these risk factors. To prevent microembolization related to PCI, thrombus aspiration appears promising, but distal protection devices have failed to demonstrate the expected results among patients with AMI. Most cardioprotective agents developed to modify the risk factors for no-reflow have been effective in animal experiments but have disappointed in clinical trials. Adjunctive treatments using statins, adenosine, atrial natriuretic peptide, nicorandil, or glycoprotein IIb/IIIa antagonists have been effective in reducing the infarct size or improving outcomes after AMI in clinical studies, although some have shown inconsistent results. It is probable that the relevance of each component associated with no-reflow is different for individual patients, and therefore the attempt to indiscriminately apply one treatment to all patients will not be as successful as expected. Individual susceptibility has to be evaluated when selecting an appropriate adjunctive treatment to prevent no-reflow in patients with AMI.

TENECTEPLASE AS A NEW MEDICATION IN MANAGING NO-REFLOW

No-reflow has been defined as “inadequate myocardial perfusion through a given segment of coronary circulation without angiographic evidence of a mechanical obstruction”. Important components of the process are thought to include endothelial ischemic injury producing “blebs” of tissue that directly obstruct the microvasculature, leukocyte plugging of capillaries, and the vascular effects of reactive oxygen species. No-reflow can complicate any percutaneous intervention (PCI), though it is more common following acute myocardial infarctions (MI), particularly with prolonged occlusion times. A 59-year-old woman presented to the hospital after two hours of continuous chest pain. Because of acute myocardial infarction of the inferior and lateral wall, she underwent direct stenting to an occlusion in the right coronary artery. Despite successful implantation of stents revascularization failed. In absence of aspiration devices and other pharmacological agent we decide to apply 30 mg (6000 IU) tenecteplase intracoronary. Three min after administration TIMI flow grade improved from TIMI 0 to TIMI 3. Managing no-reflow can be approached in a number of different ways and needs to be tailored to the type of intervention being performed. As confirmed in practice, prevention is better than cure and both mechanical and pharmacological approaches can be employed in high risk cases. In the setting of acute myocardial infarction the most effective preventative measure is the rapid opening of the vessel and as such the development of a robust and efficient primary PCI service is integral to the avoidance of this complication. Managing no-reflow will become increasingly important with the wider development of primary PCI. Within the setting of acute myocardial infarctions with no reflow as primary percutaneous intervention complication, there are potential important future pharmacological regimens that may become established and one of them can be tenecteplase. Acta Medica Medianae 2012; 51(1):42-45.

Plasma B-type natriuretic peptide level can predict myocardial tissue perfusion in patients undergoing primary percutaneous coronary intervention for acute ST-segment elevation myocardial infarction

Inadequate myocardial tissue perfusion after successful revascularization in ST-segment elevation myocardial infarction (STEMI) is associated with worse clinical outcomes. We investigated whether the plasma B-type natriuretic peptide (BNP) level on admission could predict the status of myocardial tissue perfusion in patients who underwent primary percutaneous coronary intervention (PCI). The study prospectively enrolled 102 patients with STEMI who underwent primary PCI within 12 h of symptom onset. The grade of myocardial tissue perfusion was measured by ST-segment resolution, corrected thrombolysis in myocardial infarction frame count, and myocardial blush grade after primary PCI. All-cause mortality at 1 month after PCI was assessed. All patients were divided into two groups according to the BNP level; high-BNP group (≥80 pg/ml, n=43) and low-BNP group (<80 pg/ml, n=59). High-BNP group had significantly lower ST-segment resolution (42.69 ± 24.85 vs. 71.15 ± 19.37%, P<0.001), higher corrected thrombolysis in myocardial infarction frame count (53.7 ± 19.7 vs. 44.5 ± 15.5, P=0.04), lower myocardial blush grade (2.4 ± 0.9 vs. 2.9 ± 0.3, P=0.001), and higher short-term mortality (16.2 vs. 3.3%, P=0.023). In multivariate logistic regression analysis for prediction of good myocardial tissue perfusion after PCI, the odds ratio of low-BNP group was 4.12 (95% confidence interval 1.49-13.08, P<0.01). The patients with STEMI who had higher BNP level on admission showed inadequate myocardial tissue perfusion status after primary PCI. The plasma BNP level on admission may serve as a predictor of tissue perfusion after primary PCI in patients with STEMI.

No-reflow: again prevention is better than treatment

Primary percutaneous coronary intervention (PPCI) is the preferred reperfusion strategy for treating acute ST-segment elevation myocardial infarction (STEMI). The main goals are to restore epicardial infarct-related artery patency and achieve microvascular reperfusion as early as possible, thus limiting the extent of irreversibly injured (necrotic) myocardium.1 Angiographic assessment of myocardial blood flow is reported as thrombolysis in myocardial infarction (TIMI) flow, and although TIMI flow grade relates to outcome, even in the presence of TIMI-3 flow tissue level perfusion can still be disturbed as measured by other indexes such as corrected TIMI frame count (cTFC) or more invasive measures of coronary blood flow. Thus, depending on how it is measured, inadequate tissue level reperfusion can occur in up to 50% of cases. No-reflow is the term used to describe inadequate myocardial perfusion of a given coronary segment without angiographic evidence of mechanical vessel obstruction.2 Despite optimal evidence-based PPCI, myocardial no-reflow can still occur, negating many of the benefits of restoring culprit vessel patency, and is associated with a worse in-hospital and long-term prognosis.2 It is important to outline that no-reflow is only one of the four types of cardiac dysfunction (myocardial stunning, no-reflow, reperfusion arrhythmias, and lethal reperfusion injury) caused by myocardial reperfusion as recently summarized by Yellon and Hausenloy,3 and it refers to the high impedance of microvascular blood flow encountered during opening of the infarct-related coronary artery. In this manuscript, we concentrate on the processes of no-reflow while recognizing the relationships with reperfusion injury and the complexity of each of the interactions involved. The multifactorial nature of no-reflow has been summarized recently into four interacting processes: ischaemic injury, reperfusion injury, distal embolization, and susceptibility of microcirculation to injury ( Figure 1 ).4 Ischaemia–reperfusion (IR) injury is central to the pathophysiology of no-reflow and is associated …

Stress Test Intensity and ECG Correlation With Nuclear Imaging

INTRODUCTION: Changes in the ECG during exercise can indicate inadequate myocardial perfusion. Elevation and depression of the ST segment are the most commonly used indicators of ischemia. Their sensitivity tends to correlate with the intensity of exercise and stress on the heart. Previous research has shown that stress ECG sensitivity decreases when stress is less than 100% HR max and falls off markedly below 85% HR max. The use of age estimated HR max is appropriate for groups but not for individuals because of the normal distribution of HR max in the adult population. PURPOSE: To determine the frequency of true maximum stress tests and the frequency of discrepancies between ECG and nuclear imaging in a clinical setting. METHODS: Heart Rate during the final two stages and ST changes in the final stage of 100 sequential Bruce protocol treadmill stress tests with nuclear imaging were retrospectively identified for individuals not on a chronotropic medication. The official ECG and nuclear imaging interpretations were compared. Maximum stress tests were determined by a HR increase of <5 beats per minute in the final stage compared to the previous stage. Simple percentages of tests meeting criteria and correlation of ECG and nuclear imaging readings were calculated. RESULTS: Only 8% of subjects plateaued HR between the final two stress test stages, and only 14% plateaued within the final stage. 82% were not able to attain their age estimated maximum HR. Criteria for ischemia were met in 12% of the ECG's and 18% of the nuclear images. There were discrepancies between ECG and nuclear images in 22 cases. CONCLUSIONS: There is a low incidence of true maximum stress tests in this clinical setting; therefore, it is difficult, if not impossible, to ascertain the accuracy of stress ECG or nuclear imaging because the level of stress is unknown.