Flow In Culprit Artery Research Articles

Role of fibrinogen, albumin and fibrinogen to albumin ratio in determining angiographic severity and outcomes in acute coronary syndrome.

Coronavirus disease 2019 (COVID-19) pandemic unmasked the huge deficit in healthcare resources worldwide. It highlighted the need for efficient risk stratification in management of cardiovascular emergencies. To study the applicability of the old, available and affordable nonconventional biomarkers: albumin and fibrinogen in their ability to predict angiographic severity and clinical outcomes in patients with acute coronary syndrome (ACS). In this prospective, observational study, 166 consecutive patients with ACS were enrolled. Fibrinogen, albumin and their ratio were determined from serum. Patients with underlying chronic liver disease, active malignancy, autoimmune disease, active COVID-19 infection and undergoing thrombolysis were excluded. Mean age of the population was 60.5 ± 1.5 years, 74.1% being males. ST elevation myocardial infarction (STEMI) was most common presentation of ACS seen in 57% patients. Fibrinogen albumin ratio (FAR) ≥ 19.2, had a sensitivity of 76.9% and specificity of 78.9 % [area under the receiver operating characteristic curves (AUROC) = 0.8, P = 0.001] to predict ≤ thrombolysis in myocardial infarction (TIMI) 1 flow in culprit artery in STEMI patients. Even in non-STEMI patients, FAR ≥ 18.85 predicted the same with 80% sensitivity and 63% specificity (AUROC = 0.715, P = 0.006). Novel biomarkers, with their high cost, lack of availability and long turn over time are impractical for real-world use. Identifying ≤ TIMI 1 flow in the culprit artery has significant impact of management and outcome. Our study has shown that readily available biomarkers like fibrinogen and albumin can help identify these high-risk patients with good accuracy. This allows risk-stratification and individualization of treatment in ACS.

Predictors of Survival and Ventricular Recovery Following Acute Myocardial Infarction Requiring Extracorporeal Membrane Oxygenation Therapy.

The use of venoarterial extracorporeal membrane oxygenation (VA-ECMO) following acute myocardial infarction with cardiogenic shock (AMI-CS) is increasing, but the ability to predict favorable outcomes with support remains limited. We retrospectively reviewed all patients with AMI-CS supported with VA-ECMO between December 2008 and June 2018. One hundred twenty-six patients received VA-ECMO for AMI-CS during the study period; of these, 39 (31.0%) experienced ventricular recovery and were discharged while 87 (69.0%) did not recover, with 71 (56.3%) dying in the hospital and 16 (12.7%) surviving to discharge with either left ventricular assist device or heart transplant. TIMI 3 flow in culprit artery (OR, 4.01; 95% CI, 1.25-12.77; p = 0.02), serum lactate (OR, 0.89; 95% CI, 0.80-0.99; p = 0.04), and prompt revascularization (OR, 3.39; 95% CI, 1.18-9.81; p = 0.02) were independent predictors of ventricular recovery. Four variables emerged as independent predictors of in-hospital mortality and were used to create the AMI-ECMO Risk Score: age >70 years, creatinine >1.5 mg/dL, serum lactate > 4.0 mmol/L, and lack of TIMI 3 flow in culprit artery. In patients supported with VA-ECMO for AMI-CS, prompt, successful revascularization, and lower serum lactate were associated with ventricular recovery while younger age, lower serum lactate, and creatinine, and successful revascularization were associated with survival to discharge. The AMI-ECMO risk score is a simple tool that can help risk stratify patients with AMI-CS being considered for VA-ECMO support.

Prehospital Adenosine Diphosphate Receptor Blocker Use, Culprit Artery Flow, and Mortality in STEMI: The MADDEC Study.

Background and ObjectiveThe newer adenosine diphosphate (ADP) receptor blockers ticagrelor and prasugrel are superior to clopidogrel in the long-term management of acute coronary syndrome (ACS). We evaluated the acute performance (prehospital loading) of these ADP receptor blockers in a primary percutaneous coronary intervention (PCI) for an ST-elevation myocardial infarction (STEMI).MethodsIn a retrospective, single-center registry study, data on all STEMI patients admitted for their first primary PCI between January 2007 and April 2020 were analyzed (n = 3218). The three ADP receptor blockers were mainly used during consecutive periods (clopidogrel 2007–2010, prasugrel 2011–2014, and ticagrelor 2014–2020), and were compared with risk factor-adjusted multivariate logistic regression for acute 3- and 7-day mortality and culprit artery flow before and after PCI.ResultsOf the 3218 total patients, 47.6% (n = 1532) were treated with ticagrelor, 22.1% (n = 711) were treated with prasugrel, and 30.3% (n = 975) were treated with clopidogrel. The use of ticagrelor or prasugrel as opposed to clopidogrel was associated with better culprit artery flow before PCI (odds ratio [OR] 1.21 for moderate or good flow, 95% confidence interval [CI] 1.03–1.42, p = 0.022), as well as lower acute mortality (OR 0.66 for 3-day mortality, 95% CI 0.46–0.95, p = 0.025; and OR 0.71 for 7-day mortality, 95% CI 0.52–0.98, p = 0.039). The results in regard to acute mortality were highlighted among patients with short treatment delays (disappearing with longer treatment delays; p < 0.05 for interaction).ConclusionsThe newer ADP receptor blockers are associated with lower mortality and better culprit artery flow at presentation when compared with clopidogrel. There are no significant differences between the two newer drugs. As the drugs were mainly used during three consecutive periods, unmeasured confounding related to the development of cardiac care and changes in the population may contribute to the results.Supplementary InformationThe online version contains supplementary material available at 10.1007/s40261-021-01045-2.

Effect of coronary flow on intracoronary alteplase: a prespecified analysis from a randomised trial

ObjectivesPersistently impaired culprit artery flow (<TIMI 3) during primary percutaneous coronary intervention is a surrogate for failed myocardial perfusion. We evaluated the effects of intracoronary alteplase according to TIMI flow...

Noninvasive Evaluation of Coronary Perfusion by Transthoracic Doppler Echocardiography in Patients with Anterior Myocardial Infarction before Coronary Intervention

Background: Transthoracic Doppler Echocardiography (TTDE) has made a breakthrough in noninvasive evaluation of coronary artery flow, especially in the distal left anterior descending coronary artery (LAD). The present study was intended to test the hypothesis whether TTDE can differentiate coronary perfusion with Thrombolysis in Myocardial Infarction (TIMI) grade 3 from TIMI grade ≤2 in patients with anterior myocardial infarction (AMI). Methods: A total of 30 consecutive patients suggestive of anterior MI including those who received thrombolysis with the potential need for Percutaneus Coronary Intervention (PCI) were enrolled in the study. The coronary perfusion was evaluated by antegrade flow visualization in distal LAD by Colour TTDE and antegrade flow velocity measured by pulsed TTDE followed by coronary angiogram for TIMI grade flow in culprit artery. The sensitivity, specificity and diagnostic accuracy were determined by comparing TTDE parameters with angiographic TIMI flow grade. Results: The antegrade distal LAD flow visualization by Color TTDE enabled differentiation of TIMI 3 from TIMI ≤2 with a sensitivity, specificity, PPV, NPV and diagnostic accuracy of 100%, 62.5%, 40%, 100% and 70% respectively. The Receiver Operating Characteristic (ROC) curve constructed to find the cut-off value for antegrade flow velocity in distal LAD in differentiating TIMI 3 from TIMI 0-2 was found to be 30.5 cm/ s with an area under the curve being 0.893, p =0.011. The antegrade flow velocity in distal LAD e” 30.5 cm/s by pulsed TTDE had a fair sensitivity (66.7%) , but had high specificity (100%) and overall diagnostic accuracy (86.7%). Conclusion: The study concluded that antegrade distal LAD flow visualization by Color TTDE can fairly differentiate TIMI 3 from TIMI ≤2 with high sensitivity, and moderate specificity and diagnostic accuracy. Additionally, the antegrade flow velocity in distal LAD by pulsed TTDE has a moderate sensitivity and high specificity to predict the angiographic TIMI flow grade. Thus, TTDE enables noninvasive differentiation of coronary perfusion in patients with anterior MI before coronary intervention.&#x0D; University Heart Journal Vol. 15, No. 1, Jan 2019; 22-27

Predictors of Survival to Discharge and Ventricular Recovery after VA-ECMO Support for Acute Myocardial Infarction Complicated by Cardiogenic Shock

Purpose The use of veno-arterial extra-corporeal membrane oxygenation (VA-ECMO) following acute myocardial infarction (AMI) with cardiogenic shock (CS) is increasing, but the ability to predict favorable clinical response is limited. We investigated predictors of in hospital mortality and ventricular recovery in patients supported with VA-ECMO for AMI-CS. Methods We retrospectively reviewed charts of patients with AMI who were supported with VA-ECMO from 2007-2018. Data collected included AMI characteristics and measures of cardiac function. Logistic regression was used to identify predictors of survival to discharge and recovery which was defined as survival to discharge without heart replacement therapy (HRT, durable LVAD or transplant). Results 137 patients were treated with VA-ECMO for AMI during the study period. Mean cardiac index at implantation in the cohort was 1.82 ±0.53 and 26 patients (18.9%) had VA-ECMO placed during active CPR. 43 patients (31.4%) were supported with IABP either before or during VA-ECMO support; 75 patients (54.7%) were supported with Impella either before or during VA-ECMO support. 30-day survival was 60.6% and 52.6% survived to discharge. Of the 72 patients surviving to discharge, 26 (36.1%) were discharged with HRT and 46 (63.9%) had recovery. In a multivariable analysis including, age, gender, lactate, TIMI 3 flow in culprit artery, and LV ejection fraction, younger age was the only independent predictor of survival to discharge (OR 1.18, p=0.02). Independent predictors of ventricular recovery were presence of TIMI 3 flow in culprit artery (OR 5.45, p=0.03) and residual CAD (OR 0.22, p=0.04, Table). At a median follow-up of 375 days (IQR 112, 959) after discharge, 2/46 (4.3%) patients required HRT. Conclusion In patients supported with VA-ECMO for AMI-CS, younger age was associated with survival to discharge while markers of successful revascularization were associated with ventricular recovery.

5 Relationships between infarct zone extracellular volume and clinical measures of ischaemia and reperfusion in acute STEMI survivors: Abstract 5 Table 1

<h3>Background</h3> The clinical significance of infarct extracellular volume (ECV) post-STEMI is unknown. ECV can be estimated by cardiac magnetic resonance imaging (CMR) using T1 MOLLI maps. We measured infarct ECV in STEMI survivors, and assessed the relationships between ECV and markers of MI severity. <h3>Methods</h3> STEMI survivors were enrolled in a single-centre cohort study (BHF MR-MI study – NCT02072850). Culprit artery flow was described by thrombus in myocardial infarction (TIMI) classification. CMR was performed at 1.5 Tesla (Siemens MAGNETOM Avanto) 2-days and 6-months post-MI, including T1-mapping with MOLLI before and 15-minutes after contrast (0.15 mmol/kg gadoterate meglumine). ECV was analysed by outlining regions-of-interest (ROIs) in infarcted myocardium, including microvascular obstruction, and left ventricular (LV) blood pool. ECV was calculated as the relaxation rate (R1=1/T1) for myocardium and LV blood pool before vs. after contrast, corrected for haematocrit. ECV was compared with TIMI-flow pre- and post-percutaneous coronary intervention (PCI) and ST-segment resolution. A reduction in ST-segment voltage of ≥70% was considered complete ST-resolution and &lt;70% was considered incomplete ST-resolution. <h3>Results</h3> 201 STEMI patients (age 58 ± 11 years; 156 (77%) male) were enrolled. Infarct ECV was similar at baseline and follow-up (51.3 ± 9.5% vs. 50.3 ± 12.0%, p = 0.1). Pre-PCI, 131 (65%) patients had TIMI-flow 0 and 70 (35%) had TIMI-flow 1–3. Post-PCI, 3 (1.5%) patients had TIMI-flow 0 and 198 (98.5%) had TIMI-flow 2–3. TIMI-flow 0 pre-PCI was associated with higher infarct ECV at baseline (p &lt; 0.001) and follow-up (p = 0.004). TIMI-flow post-PCI was not associated with infarct ECV. ST-resolution was complete in 104 (52%) patients and incomplete in 96 (48%) patients. Incomplete ST-resolution was associated with higher infarct ECV at baseline (p = 0.001) and follow-up (p = 0.026) (Table 1). <h3>Conclusion</h3> Preserved culprit artery flow and complete ST-resolution are associated with lower infarct ECV at baseline and follow-up. Clinical and electrocardiographic markers of MI severity are predictors of interstitial expansion in the infarct zone in STEMI patients.

Usefulness of the QRS Score as a Strong Prognostic Marker in Patients Discharged After Undergoing Primary Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction

The prognostic value of myocardial infarct size estimation by QRS scoring in patients with ST-segment elevation myocardial infarction (STEMI) who undergo primary percutaneous coronary intervention (PCI) is unclear. The standard 32-point Selvester QRS score on the discharge electrocardiogram (each point approximately 3% left ventricular mass) was calculated in 4,113 patients with STEMI who underwent primary PCI and survived to hospital discharge in the APEX-AMI trial. QRS scores were divided into tertiles, i.e., < or =3 (<10% myocardium), 4 to 7 (10% to 21% myocardium), and > or =8 (>21% myocardium). Adjusted associations between QRS score and 90-day outcomes (death and composite of death/congestive heart failure (CHF)/shock) were examined. Higher QRS scores were associated with male gender, higher heart rate, worse Killip class, noninferior infarct location, greater ST-segment deviation, and longer times to reperfusion. Higher QRS scores were also associated with impaired culprit artery flow before and after PCI and more frequent multivessel disease. Adverse outcomes occurred more often in patients with higher QRS scores (90-day death: 1.9%, QRS score 0 to 3; 3.4%, 4 to 7; 4.9%, > or =8; 90-day death/shock/CHF: 4.5%, 0-3; 7.8%, 4 to 7; 12.1%, > or =8). After multivariable adjustment, patients with higher QRS scores remained more likely to develop an adverse outcome versus those with QRS scores < or =3 (score 4 to 7, hazard ratios [HR] for death 2.08, 95% confidence interval [CI] 1.26 to 3.41; HR for death/CHF/shock 2.00, 95% CI 1.26 to 3.17; score > or =8, HR for death 2.57, 95% CI 1.56 to 4.24, HR for death/CHF/shock 2.93, 95% CI 1.84 to 4.67). In conclusion, infarct size as estimated by QRS scoring at hospital discharge is an independent and prognostically relevant metric in patients with STEMI undergoing primary PCI.

Predictive value of preprocedure NTProBNP level for development of no reflow/slow flow phenomenon

Background: Recently it has been shown that elevated NTProBNP levels were associated with more severe CAD, slower blood flow in culprit artery and more proximal lesions in the coronary artery. Outcomes following PCI depend upon lesion morphology and slow/noreflow phenomenon which occurs in 5–25% cases. Various risk scores, e.g. MAYO risk score have been devised to predict outcome after PCI, however data comparing NTProBNP levels with various risk scores especially in the setting of slow/noreflow are lacking.

Global impairment of coronary blood flow in the setting of acute coronary syndromes (a RESTORE substudy)

Acute coronary syndromes result in a global impairment of coronary blood flow with nonculprit artery blood flow being associated with culprit artery flow and vice versa. Improvements in nonculprit artery flow are related to improvements in culprit artery flow after percutaneous intervention; nonculprit arteries with abnormal flow sustain greater improvements in their flow after culprit artery intervention.

Weight-adjusted dosing of TNK-tissue plasminogen activator and its relation to angiographic outcomes in the thrombolysis in myocardial infarction 10B trial

Fixed doses of thrombolytic agents are generally administered to patients of varying body weights, and the dose-response relation may be confounded by the variability in patient weight. We hypothesized that higher doses of TNK-tissue plasminogen activator (tPA) per unit body weight would be related to improved flow at 90 minutes after thrombolytic administration. A total of 886 patients with acute myocardial infarction were randomized to receive either a single bolus of 30, 40, or 50 mg of TNK-tPA or front-loaded tPA in the Thrombolysis In Myocardial Infaction (TIMI) 10B trial. The dose of TNK-tPA administered was divided by the patient’s weight to arrive at the TNK-tPA dose (mg) per unit body weight (kg), and patients were stratified into tertiles based on mg/kg of TNK-tPA: low dose, 0.2 to 0.39 mg/kg; mid-dose, 0.40 to 0.51 mg/kg; high dose, 0.52 to 1.24 mg/kg. Flow in the culprit and nonculprit arteries was analyzed using the TIMI flow grades and the corrected TIMI frame count (CTFC). The median CTFC in culprit arteries differed between the tertiles (3-way p = 0.007), with the CTFC being 7.2 frames faster in high-dose than in low-dose patients (43.1 ± 30.1, median 31.2, n = 171 vs 54.6 ± 34.8, median 38.4, n = 166, 2-way p = 0.002). Patients in the mid- and high-dose tertiles achieved patency more frequently (TIMI grade 2 or 3 flow) by 60 minutes (p = 0.02), and the 90-minute percent diameter stenosis was less severe in patients in the high- versus low-dose tertile (p = 0.03). In nonculprit arteries, the CTFC was faster in high- than in low-dose tertiles (29.6 ± 13.4, median 26.9, n = 130 vs 34.7 ± 16.3, median 32.8, n = 108, 3-way p = 0.03, 2-way p = 0.008). In patients who underwent percutaneous transluminal coronary angioplasty (PTCA), the CTFC in culprit arteries after PTCA was fastest in the high- and mid-dose tertiles than in those receiving low doses (2- way p = 0.05). Thus, higher doses per unit body weight of TNK-tPA result in not only faster culprit artery flow, but also faster nonculprit, global, and post-PTCA flow, which may reflect earlier opening, reduced stunning, or improved microvascular function. The greater effectiveness of thrombolysis must be weighed against any increase in risk.

Impaired coronary blood flow in nonculprit arteries in the setting of acute myocardial infarction

OBJECTIVES AND BACKGROUNDWhile attention has focused on coronary blood flow in the culprit artery in acute myocardial infarction (MI), flow in the nonculprit artery has not been studied widely, in part because it has been assumed to be normal. We hypothesized that slower flow in culprit arteries, larger territories infarcted and hemodynamic perturbations may be associated with slow flow in nonculprit arteries.METHODSThe number of frames for dye to first reach distal landmarks (corrected TIMI [Thrombolysis in Acute Myocardial Infarction] frame count [CTFC]) were counted in 1,817 nonculprit arteries from the TIMI 4, 10A, 10B and 14 thrombolytic trials.RESULTSNonculprit artery flow was slowed to 30.9 ± 15.0 frames at 90 min after thrombolytic administration, which is 45% slower than normal flow in the absence of acute MI (21 ± 3.1, p < 0.0001). Patients with TIMI grade 3 flow in the culprit artery had faster nonculprit artery CTFCs than those patients with TIMI grades 0, 1 or 2 flow (29.1 ± 13.7, n = 1,050 vs. 33.3 ± 16.1, n = 752, p < 0.0001). The nonculprit artery CTFC improved between 60 and 90 min (3.3 ± 17.9 frames, n = 432, p = 0.0001), and improvements were related to improved culprit artery flow (p = 0.0005). Correlates of slower nonculprit artery flow included a pulsatile flow pattern (i.e., systolic flow reversal) in the nonculprit artery (p < 0.0001) and in the culprit artery (p = 0.01), a left anterior descending artery culprit artery location (p < 0.0001), a decreased systolic blood pressure (p = 0.01), a decreased ventriculographic cardiac output (p = 0.02), a decreased double product (p = 0.0002), a greater percent diameter stenosis of the nonculprit artery (p = 0.01) and a greater percent of the culprit artery bed lying distal to the stenosis (p = 0.04). Adjunctive percutaneous transluminal coronary angioplasty (PTCA) of the culprit artery restored a culprit artery CTFC (30.4 ± 22.2) that was similar to that in the nonculprit artery at 90 min (30.2 ± 13.5), but both were slower than normal CTFCs (21 ± 3.1, p < 0.0005 for both). If flow in the nonculprit artery was abnormal (CTFC ≥ 28 frames) then the CTFC after PTCA in the culprit artery was 17% slower (p = 0.01). Patients who died had slower global CTFCs (mean CTFC for the three arteries) than patients who survived (46.8 ± 21.3, n = 47 vs. 39.4 ± 16.7, n = 1,055, p = 0.02).CONCLUSIONSAcute MI slows flow globally, and slower global flow is associated with adverse outcomes. Relief of the culprit artery stenosis by PTCA restored culprit artery flow to that in the nonculprit artery, but both were 45% slower than normal flow.