The association of atherogenic index of plasma with cardiovascular outcomes in patients with coronary artery disease: A systematic review and meta-analysis.

BACKGROUND: Atherogenic index of plasma (AIP) represents a novel marker in the current era of cardiovascular diseases. In this meta-analysis, we aimed to evaluate the association of AIP with cardiovascular prognosis in patients with coronary artery disease (CAD). METHODS: PubMed, Scopus, and Web of Science databases were searched from inception through 2024. The primary outcome was major cardiovascular events (MACE). The secondary outcomes included all-causes death, cardiovascular death, myocardial infarction (MI), stroke, revascularization, and no-reflow phenomenon. AIP was determined by taking the logarithm of the ratio of triglyceride (TG) to high-density lipoprotein cholesterol (HDL-C). The data analysis was represented using the risk ratio (RR) along with a 95% confidence interval (CI). RESULTS: Sixteen studies with a total number of 20,833 patients met the eligible criteria. The pooled-analysis showed a significant increased risk of MACE in the highest AIP group compared with the lowest AIP group (RR = 1.63; 95% CI, 1.44-1.85; P < 0.001). A similar result was observed when AIP was regarded as a continuous variable (RR = 1.54; 95% CI, 1.30-1.83; P < 0.001). Besides, elevated AIP was associated with increased risk of cardiovascular death (RR = 1.79; 95% CI, 1.09-2.78; P = 0.02), MI (RR = 2.21; 95% CI, 1.55-3.13; P < 0.001), revascularization (RR = 1.62; 95% CI, 1.34-1.97; P < 0.001), no-reflow phenomenon (RR = 3.12 95% CI, 1.09-8.96; P = 0.034), and stent thrombosis (RR = 13.46; 95%CI, 1.39-129.02; P = 0.025). However, AIP was not significantly associated with the risk of all-causes death and stroke among patients with CAD. CONCLUSIONS: The results of this study demonstrated that increased AIP is an independent prognostic factors in patients with CAD. Further research is warranted to elucidate the potential development of targeted interventions to modify AIP levels and improve patient outcomes.

No-Reflow Prediction in Acute Coronary Syndrome During Percutaneous Coronary Intervention: The NORPACS Risk Score.

BACKGROUND: Suboptimal coronary reperfusion (no reflow) is common in acute coronary syndrome percutaneous coronary intervention (PCI) and is associated with poor outcomes. We aimed to develop and externally validate a clinical risk score for angiographic no reflow for use following angiography and before PCI. METHODS: We developed and externally validated a logistic regression model for prediction of no reflow among adult patients undergoing PCI for acute coronary syndrome using data from the Melbourne Interventional Group PCI registry (2005-2020; development cohort) and the British Cardiovascular Interventional Society PCI registry (2006-2020; external validation cohort). RESULTS: A total of 30 561 patients (mean age, 64.1 years; 24% women) were included in the Melbourne Interventional Group development cohort and 440 256 patients (mean age, 64.9 years; 27% women) in the British Cardiovascular Interventional Society external validation cohort. The primary outcome (no reflow) occurred in 4.1% (1249 patients) and 9.4% (41 222 patients) of the development and validation cohorts, respectively. From 33 candidate predictor variables, 6 final variables were selected by an adaptive least absolute shrinkage and selection operator regression model for inclusion (cardiogenic shock, ST-segment-elevation myocardial infarction with symptom onset >195 minutes pre-PCI, estimated stent length ≥20 mm, vessel diameter <2.5 mm, pre-PCI Thrombolysis in Myocardial Infarction flow <3, and lesion location). Model discrimination was very good (development C statistic, 0.808; validation C statistic, 0.741) with excellent calibration. Patients with a score of ≥8 points had a 22% and 27% risk of no reflow in the development and validation cohorts, respectively. CONCLUSIONS: The no-reflow prediction in acute coronary syndrome risk score is a simple count-based scoring system based on 6 parameters available before PCI to predict the risk of no reflow. This score could be useful in guiding preventative treatment and future trials.

No-reflow after stroke reperfusion therapy: An emerging phenomenon to be explored.

In the field of stroke thrombectomy, ineffective clinical and angiographic reperfusion after successful recanalization has drawn attention. Partial or complete microcirculatory reperfusion failure after the achievement of full patency of a former obstructed large vessel, known as the "no-reflow phenomenon" or "microvascular obstruction," was first reported in the 1960s and was later detected in both experimental models and patients with stroke. The no-reflow phenomenon (NRP) was reported to result from intraluminal occlusions formed by blood components and extraluminal constriction exerted by the surrounding structures of the vessel wall. More recently, an emerging number of clinical studies have estimated the prevalence of the NRP in stroke patients following reperfusion therapy, ranging from 3.3% to 63% depending on its evaluation methods or study population. Studies also demonstrated its detrimental effects on infarction progress and neurological outcomes. In this review, we discuss the research advances, underlying pathogenesis, diagnostic techniques, and management approaches concerning the no-reflow phenomenon in the stroke population to provide a comprehensive understanding of this phenomenon and offer references for future investigations.

The predictive value of the HALP score for no-reflow phenomenon and short-term mortality in patients with ST-elevation myocardial infarction.

OBJECTIVE: ST-elevation myocardial infarction (STEMI) is a medical emergency demanding immediate intervention, and primary percutaneous coronary intervention (pPCI) is the standard of care for this condition. While PCI has proven highly effective, a subset of patients experience the devastating no-reflow phenomenon, and some face increased short-term mortality. The Hemoglobin, Albumin, Lymphocyte, and Platelet (HALP) score, a novel biomarker-based tool, has recently surfaced as an innovative predictor of these adverse outcomes. This study aims to investigate the groundbreaking findings that designate a low HALP score as a robust risk factor for no-reflow and short-term mortality in STEMI patients. METHODS: 1817 consecutive STEMI patients who underwent pPCI were included in this retrospective study, and the patients were divided into two groups according to whether no-reflow developed or not, and the HALP scores of the groups were compared. In addition, short-term mortality was compared between the study groups according to their HALP score values. The predictive ability of the HALP score for no-reflow was evaluated using a receiver operating characteristic curve. RESULTS: No-reflow developed in 198 (10.1%) of the patients included in the study. HALP score value was found to be significantly lower in the no-reflow group (27 ± 13 vs 47 ± 24, p < 0.001). After multivariable adjustment, the HALP score was an independent predictor of no-reflow (OR, 0.923, 95% CI, 0.910-0.935, p < 0.001). Furthermore, the HALP score showed good discrimination for no-reflow (AUC, 0.771, 95% CI, 0.737-0.805, p < 0.001). In addition, HALP score was determined to be an independent predictor for short-term mortality (HR, 0.955, 95% CI, 0.945-0.966, p < 0.001). CONCLUSIONS: HALP score can independently predict the development of no-reflow and short-term mortality in STEMI patients undergoing pPCI.

The predictive value of laboratory parameters for no-reflow phenomenon in patients with ST-elevation myocardial infarction following primary percutaneous coronary intervention: A meta-analysis.

To date, the predictive role of laboratory indicators for the phenomenon of no flow is unclear. Hence, our objective was to conduct a meta-analysis to investigate the association between laboratory parameters and the risk of the no-reflow phenomenon in patients with ST-elevation myocardial infarction (STEMI) following primary percutaneous coronary intervention (PCI). This, in turn, aims to offer valuable insights for early clinical prediction of no-reflow. We searched Pubmed, Embase, and Cochrane Library from the establishment of the database to October 2023. We included case-control or cohort study that patients with STEMI following primary PCI. We excluded repeated publication, research without full text, incomplete information or inability to conduct data extraction and animal experiments, reviews, and systematic reviews. STATA 15.1 was used to analyze the data. The pooled results indicated that elevated white blood cell (WBC) count (odds ratio [OR] = 1.061, 95% confidence interval [CI]: 1.013-1.112), neutrophil count (OR = 1.324, 95% CI: 1.128-1.553), platelet (PLT) (OR = 1.002, 95% CI: 1.000-1.005), blood glucose (OR = 1.005, 95% CI: 1.002-1.009), creatinine (OR = 1.290, 95% CI: 1.070-1.555), total cholesterol (TC) (OR = 1.022, 95% CI: 1.012-1.032), d-dimer (OR = 1.002, 95% CI: 1.001-1.004), and fibrinogen (OR = 1.010, 95% CI: 1.005-1.015) were significantly associated with increased risk of no-reflow. However, elevated hemoglobin was significantly associated with decreased risk of no-reflow. In conclusion, our comprehensive analysis highlights the predictive potential of various parameters in assessing the risk of no-reflow among STEMI patients undergoing PCI. Specifically, WBC count, neutrophil count, PLT, blood glucose, hemoglobin, creatinine, TC,  d-dimer, and fibrinogen emerged as significant predictors. This refined risk prediction may guide clinical decision-making, allowing for more targeted and effective preventive measures to mitigate the occurrence of no-reflow in this patient population.

The non-HDL-C/HDL-C ratio is a strong and independent predictor of the no-reflow phenomenon in patients with ST-elevation myocardial infarction.

BACKGROUND: No-reflow (NR) is the inability to achieve adequate myocardial perfusion despite successful restoration of attegrade blood flow in the infarct-related artery after primary percutaneous coronary intervention. The non-HDL-C/HDL-C ratio has been shown to be superior to conventional lipid markers in predicting most cardiovascular diseases. In this study, we wanted to reveal the predictive value of the NR by comparing the Non-HDL-C/HDL-C ratio with traditional and non-traditional lipid markers in patients who underwent primary percutaneous coronary intervention (pPCI) due to ST-elevation myocardial infarction (STEMI). METHODS: A total of 1284 consecutive patients who underwent pPCI for STEMI were included in this study. Traditional lipid profiles were detected and non-traditional lipid indices were calculated. Patients were classified as groups with and without NR and compared in terms of lipid profiles. RESULTS: No-reflow was seen in 18.8% of the patients. SYNTAX score, maximal stent length, high thrombus burden, atherogenic index of plasma and non-HDL-C/HDL-C ratio were determined as independent predictors for NR (p < 0.05, for all). The non-HDL-C/HDL-C ratio predicts the development of NR in STEMI patients with 71% sensitivity and 67% specificity at the best cut-off value. In ROC curve analysis, the non-HDL-C/HDL-C ratio was superior to traditional and non-traditional lipid markers in predicting NR (p < 0.05, for all). CONCLUSION: The non-HDL-C/HDL-C ratio can be a strong and independent predictor of NR in STEMI patients and and therefore non-HDL-C/HDL-C ratio may be a useful lipid-based biomarker that can be used in clinical practice to improve the accuracy of risk assessment in patients with STEMI.

Triglyceride glucose-body mass index as a novel predictor of slow coronary flow phenomenon in patients with ischemia and nonobstructive coronary arteries (INOCA).

BACKGROUND: The triglyceride glucose-body mass index (TyG-BMI index) has been suggested as a novel predictor of insulin resistance. However, its predictive value for slow coronary flow phenomenon (SCFP) in patients with ischemia and nonobstructive coronary arteries (INOCA) remains unclear. METHODS: We consecutively recruited 1625 patients with INOCA from February 2019 to February 2023 and divided them into two groups based on thrombolysis in myocardial infarction (TIMI) frame counts (TFCs): the SCFP group (n = 79) and the control group. A 1:2 age-matched case-control study was then performed. The TyG-BMI index was calculated as ln [plasma triglyceride (mg/dL) × fasting blood glucose (mg/dL)/2] × BMI. RESULTS: TyG-BMI index in the SCFP group (218.3 ± 25.2 vs 201.0 ± 26.5, P < .001) was significantly higher than in the normal controls. TyG-BMI index also increased with the number of coronary arteries involved in the SCFP. Multivariate logistic regression analysis showed that TyG-BMI, BMI, and TG were independent predictors for SCFP. Receiver operating characteristic (ROC) curve analysis showed that when the TyG-BMI index was above 206.7, the sensitivity and specificity were 88.6% and 68.5%, respectively, with an AUC of 0.809 (95% CI: 0.756-0.863, P = .027). Combined BMI with TG, the TyG-BMI index had a better predictive value for SCFP than BMI and TG (P < .001). CONCLUSION: The TyG-BMI index was an independent predictor for SCFP in INOCA patients, and it had a better predictive value than BMI and TG.

Coronary Slow-Flow Phenomenon in Takotsubo Syndrome: The Prevalence, Clinical Determinants, and Long-Term Prognostic Impact.

Patients with takotsubo syndrome (TTS) may present coronary slow flow (CSF) in angiography performed in the acute myocardial infarction (MI). However, the detailed clinical relevance and its long-term impact remain poorly understood. Among 7771 MI patients hospitalized between 2012 and 2019, TTS was identified in 82 (1.1%) subjects. The epicardial blood flow was assessed with thrombolysis in myocardial infarction (TIMI) scale and corrected TIMI frame count (TFC), whereas myocardial perfusion with TIMI myocardial perfusion grade (TMPG). CSF was defined as TIMI-2 or corrected TFC > 27 frames in at least one epicardial vessel. CSF was identified in 33 (40.2%) TTS patients. In the CSF-TTS versus normal-flow-TTS group, lower values of left ventricular ejection fraction on admission (33.5 (25-40) vs. 40 (35-45)%, p = 0.019), more frequent midventricular TTS (27.3 vs. 8.2%, p = 0.020) and the coexistence of both physical and emotional triggers (9.1 vs. 0%, p = 0.032) were noted. Within a median observation of 55 months, higher all-cause mortality was found in CSF-TTS compared with normal-flow TTS (30.3 vs. 10.2%, p = 0.024). CSF was identified as an independent predictor of long-term mortality (hazard ratio 10.09, 95% confidence interval 2.12-48.00, p = 0.004). CSF identified in two-fifths of TTS patients was associated with unfavorable long-term outcomes.

Association between pan-immune-inflammation value and coronary slow flow phenomenon in patients with angiographically normal coronary arteries.

INTRODUCTION: Coronary slow flow phenomenon (CSFP) is characterized by the delayed contrast filling of terminal vessels of coronary arteries in the presence of normal or nearly normal epicardial coronary arteries. Given that inflammation plays a role in cardiovascular disorders, including CSFP, using peripheral blood-derived compound prognostic indexes could be a feasible way to predict the presence of CSFP. Therefore, in the present study, we evaluated the association between pan-immune-inflammation value (PIV) and the CSFP. METHODS: This single-center, retrospective study was composed of 612 patients aged over 18 years who underwent CAG for suspected stable ischemic heart disease. The association of clinical and laboratory parameters with the CSFP was evaluated with univariate and multivariate analyses. RESULTS: The median age of the patients was 54 (IQR 46-63) and 61.3% of the patients were male. The 12.6% (84/612) of the patients had CSFP, while the coronary flow was normal in the remaining 87.4% of patients. The PIV levels had moderate success for the prediction of the CSFP (AUC: 0.675, 95% CI: 0.615-0.735, p < 0.001). In multivariate analyses, male gender (OR: 4.858, 95% CI: 2.851-8.277, p < 0.001), presence of diabetes (OR: 2.672, 95% CI: 1.396-5.113, p = 0.003), lower HDL-C values (OR: 2.120, 95% CI: 1.286-3.496, p = 0.003), and higher PIV levels (OR: 2.527, 95% CI: 1.519-4.203, p < 0.001) were associated with a higher risk of CSFP. CONCLUSION: We demonstrated that a higher risk of CSFP in patients with PIV levels. If supported by prospective evidence, PIV levels could be used as a minimally invasive reflector of CSFP.

Pan-Immune-Inflammation Value Is Independently Correlated to Impaired Coronary Flow After Primary Percutaneous Coronary Intervention in Patients With ST-Segment Elevation Myocardial Infarction.

Immune-inflammatory biomarkers have been shown to be correlated with impaired coronary flow (ICF) in ST-segment elevation myocardial infarction. In this study, we assessed the relation between a novel comprehensive biomarker, pan-immune-inflammation value (PIV), and ICF after primary percutaneous coronary intervention (pPCI) in ST-segment elevation myocardial infarction. A total of 687 patients who underwent pPCI between 2019 and 2023 were retrospectively analyzed. Blood samples were collected at admission. PIV and other inflammation parameters were compared. PIV was calculated as (neutrophil count × platelet count × monocyte count)/lymphocyte count. Postprocedural coronary flow was assessed by thrombolysis in myocardial infarction (TIMI) classification. Patients were divided into 2 groups: a group with ICF defined as postprocedural TIMI 0 to 2 and a group with normal coronary flow defined as postprocedural TIMI flow grade of 3. The mean age was 61 ± 12 years, and 22.4% of the patients were women. Compared with the normal coronary flow group (median 492, interquartile range 275 to 931), the ICF group (median 1,540, interquartile range 834 to 2,909) showed significantly increased PIV (p <0.001). The optimal cutoff for the PIV was 804, as determined by receiver operating characteristic curve. The incidence of ICF was 17.0% in all patients, 6.4% in low-PIV group (<804), and 34.2% in high-PIV group (≥804). Multivariate analyses revealed that a baseline PIV ≥804 was independently associated with post-pPCI ICF (odds ratio 5.226, p <0.001). PIV was superior to neutrophil/lymphocyte ratio and platelet/lymphocyte ratio in determining ICF. In conclusion, a high-PIV was significantly associated with an increased risk of ICF after pPCI. Moreover, PIV was a better indicator of ICF than were other inflammatory markers.

A retrospective study: Association of C-reactive protein and uric acid to albumin ratio with the no-reflow phenomenon in patients with ST elevation myocardial infarction.

BACKGROUND: The no-reflow phenomenon increases mortality and morbidity in patients with ST-segment elevation myocardial infarction (STEMI). Inflammation, endothelial dysfunction, and oxidative stress play important role in its pathophysiology. We aim to evaluate the relationship between the no-reflow phenomenon and C-reactive protein (CRP) and uric acid (UA) to albumin ratio (CUAR), which is a new marker indicating all these pathophysiological mechanisms. METHODS AND RESULTS: Study population were divided into two groups as no-reflow and reflow; according to the post-procedural thrombolysis in myocardial infarction flows and myocardial blush grade. A1:4 propensity score matching was performed.CUAR was calculated by using the following formula: log10 (CRP x UA /Albumin). CUAR levels were significantly higher in patients with no-reflow than in those with reflow (P < 0.001). CUAR levels above 1.28 predicted no-reflow with higher sensitivity of 74% and specificity of 71% than all including CRP, UA and albumin (AUC = 0.80 [95%CI: 0.76-0.83], P < 0.001). In multivariate logistic regression analysis, CUAR levels above 1.28 (OR: 4.43 [3.04-6.46], 95% CI; P < 0.001) wereindependently associated with no-reflow phenomenon. CONCLUSION: Our results showed that CUAR could be a basic and available marker to predict no-reflow in patients with STEMI who underwent primary percutaneous coronary intervention.

No-reflow phenomenon in stroke patients: A systematic literature review and meta-analysis of clinical data.

BACKGROUND: The no-reflow phenomenon refers to the absence of microvascular reperfusion despite macrovascular reperfusion. AIM: The aim of this analysis was to summarize the available clinical evidence on no-reflow in patients with acute ischemic stroke. METHODS: A systematic literature review and a meta-analysis of clinical data on definition, rates, and impact of the no-reflow phenomenon after reperfusion therapy was carried out. A predefined research strategy was formulated according to the Population, Intervention, Comparison, and Outcome (PICO) model and was used to screen for articles in PubMed, MEDLINE, and Embase up to 8 September 2022. Whenever possible, quantitative data were summarized using a random-effects model. RESULTS: Thirteen studies with a total of 719 patients were included in the final analysis. Most studies (n = 10/13) used variations of the Thrombolysis in Cerebral Infarction scale to evaluate macrovascular reperfusion, whereas microvascular reperfusion and no-reflow were mostly assessed on perfusion maps (n = 9/13). In one-third of stroke patients with successful macrovascular reperfusion (29%, 95% confidence interval (CI), 21-37%), the no-reflow phenomenon was observed. Pooled analysis showed that no-reflow was consistently associated with reduced rates of functional independence (odds ratio (OR), 0.21, 95% CI, 0.15-0.31). CONCLUSION: The definition of no-reflow varied substantially across studies, but it appears to be a common phenomenon. Some of the no-reflow cases may simply represent remaining vessel occlusions, and it remains unclear whether no-reflow is an epiphenomenon of the infarcted parenchyma or causes infarction. Future studies should focus on standardizing the definition of no-reflow with more consistent definitions of successful macrovascular reperfusion and experimental set-ups that could detect the causality of the observed findings.

"No-reflow" phenomenon in acute ischemic stroke.

Acute ischemic stroke (AIS) afflicts millions of individuals worldwide. Despite the advancements in thrombolysis and thrombectomy facilitating proximal large artery recanalization, the resultant distal hypoperfusion, referred to "no-reflow" phenomenon, often impedes the neurological function restoration in patients. Over half a century of scientific inquiry has validated the existence of cerebral "no-reflow" in both animal models and human subjects. Furthermore, the correlation between "no-reflow" and adverse clinical outcomes underscores the necessity to address this phenomenon as a pivotal strategy for enhancing AIS prognoses. The underlying mechanisms of "no-reflow" are multifaceted, encompassing the formation of microemboli, microvascular compression and contraction. Moreover, a myriad of complex mechanisms warrant further investigation. Insights gleaned from mechanistic exploration have prompted advancements in "no-reflow" treatment, including microthrombosis therapy, which has demonstrated clinical efficacy in improving patient prognoses. The stagnation in current "no-reflow" diagnostic methods imposes limitations on the timely application of combined therapy on "no-reflow" post-recanalization. This narrative review will traverse the historical journey of the "no-reflow" phenomenon, delve into its underpinnings in AIS, and elucidate potential therapeutic and diagnostic strategies. Our aim is to equip readers with a swift comprehension of the "no-reflow" phenomenon and highlight critical points for future research endeavors.

The Association Between Atherogenic Index of Plasma and No-Reflow Phenomenon in Acute Coronary Syndrome.

BACKGROUND: The atherogenic index of plasma (AIP) is a biomarker of plasma atherogenicity. Elevated AIP is linked with adverse cardiac events. We sought to examine the association of admission AIP and no-reflow phenomenon (NRP) in acute coronary syndrome (ACS) patient population treated with percutaneous coronary intervention (PCI). METHODS: Eight hundred eight-four ACS patients were included to statistical tests retrospectively and classified according to the occurrence of NRP: NRP (-) (n = 662) and NRP (+) (n = 186). AIP levels were calculated through the formula log10 (triglyceride-to-high-density lipoprotein cholesterol ratio). RESULTS: AIP levels were higher in NRP (+) patients compared to NRP (-) group patients. The receiver operating characteristic (ROC) curve analysis for AIP to predict NRP yielded an area under the ROC curve value 0.643 [95% confidence interval (CI): 0.596-0.690, P <.001]. AIP was associated with NRP in univariate logistic regression analysis [Odds Ratio (OR): 2.46; P =.001; CI: 1.44 (lower limit)-4.21 (upper limit)]. However, AIP did not emerge as a significant prognostic factor of NRP in multiple logistic regression analysis [OR: 2.11; P =.422; CI: 0.34 (lower limit)-13.11 (upper limit)]. On the other hand, peak troponin T (log10) was an independent prognostic factor for NRP [OR: 0.13; P <.001; CI: 0.10 (lower limit)-0.37 (upper limit)] occurrence. CONCLUSION: The AIP level on admission is not a statistically significant prognostic factor of NRP. However, peak troponin T (log10) is an independent prognostic parameter of NRP.

The Relationship Between TIMI Flow and MAPH Score in Patients Undergoing Primary Percutaneous Coronary Intervention for STEMI.

The MAPH (mean platelet volume, age, total protein and hematocrit) score is a newly developed simple scoring system for patients with STEMI that has been associated with satisfactory predictive values to determine thrombus burden in STEMI patients. Therefore, the aim of our study was to determine the relationship between the MAPH risk score and TIMI flow in patients with STEMI.The study included 260 patients who underwent primary percutaneous coronary intervention between December 2019 to July 2022, and had TIMI 0 flow in the responsible coronary artery due to STEMI. According to the TIMI flow score after stent implantation, the patients were classified into either the no-reflow group (n = 59) or the normal flow group (n = 201). In order to calculate the MAPH score, ROC analysis was performed to find the cutoff point for each component of the MAPH score. MAPH scores were calculated (MPV + Age + Protein + Hematocrit) for both groups. Our study was a retrospective, observational study.In the multivariable regression analysis, the MAPH score (OR: 0.567; 95%CI: 0.330-0.973, P = 0.04) and glycoprotein IIb/IIIa inhibitors (OR: 0.249; 95%CI: 0.129-0.483, P < 0.001) were parameters found to be independent predictors of TIMI flow. An MAPH score value > 2.5 predicted the presence of low TIMI coronary flow in patients with STEMI, with 78% specificity and 45% sensitivity (ROC area under curve: 0.691, 95% CI: 0.617-0.766, P < 0.001).The MAPH risk score is simple, inexpensive, and quick to calculate. A high MAPH score may be an indicator of coronary no-reflow in patients with STEMI.

Changes of left atrial morphology and function evaluated with four-dimensional automated left atrial quantification echocardiography in patients with coronary slow flow phenomenon and preserved left ventricular ejection fraction.

BACKGROUND: Coronary slow flow phenomenon (CSFP) can cause left ventricular diastolic dysfunction (LVDD). In multiple studies, the left atrial (LA) strain has been reported to be an excellent parameter for assessing LVDD. The 4-dimensional automated LA quantification (4D Auto LAQ) dedicated to the LA was recently available. Our study aimed to evaluate subclinical changes in LA morphology and function with 4D Auto LAQ in patients with CSFP and preserved left ventricular ejection fraction (LVEF). METHODS: Forty-eight patients with CSFP confirmed with coronary angiography and 46 age and gender-matched controls with normal coronary flow were enrolled. The thrombolysis in myocardial infarction frame count (TFC) method was used to record coronary blood flow velocities for each major coronary artery. LA volume, LA longitudinal and circumferential strains during each of the three LA phases (reservoir, conduit, and contraction), LA total emptying fraction (LATEF), LA active emptying fraction (LAAEF), and LA passive emptying fraction (LAPEF) were quantified with 4D Auto LAQ analysis. RESULTS: Compared with controls, LA longitudinal reservoir strain (LASr), LA longitudinal strain during the conduit phase (LAScd), LA contraction strain (LASct), LA conduit circumferential strain (LAScd-c), LATEF, LAPEF decreased significantly in individuals with CSFP. Of the 4D- LAQ parameters, only LASr [odds ratio (OR): 0.773, P < 0.001] and LATEF [OR: 0.762, P < 0.001] were associated with CSFP in multivariate analysis. A LASr ≤23.00% can differentiate CSFP from controls [sensitivity, 66.7%; specificity, 93.5%; area under the curve (AUC), 0.823; P < 0.001]. A LASr of ≤19.00% could predict the elevation of LV filling pressure in the CSFP cohort [sensitivity, 76.9%; specificity, 74.3%; area under the curve (AUC), 0.792; P < 0.001]. LASr was the only index to demonstrate significant changes compared to controls in single-vessel CSFP. Compared to the right coronary artery (RCA) and left circumflex (LCX), TFC of the left anterior descending (LAD) artery was the only independent variable of LASr (Standardized Coefficients: -0.386, P = 0.037). CONCLUSIONS: Impairment of LA reservoir function reflected by changes in LASr and LATEF can be seen in patients with CSFP. LASr could predict the elevation of LV filling pressure in CSFP individuals. LASr is more sensitive than LATEF in detecting LA reservoir dysfunction in single-vessel CSFP. CSFP in LAD exerts a more prominent influence on LASr than RCA or LCX.

Secondary rotational atherectomy is associated with reduced occurrence of prolonged ST-segment elevation following ablation.

Elevation of the ST segment after percutaneous coronary intervention (PCI) using rotational atherectomy (RA) for severely calcified lesions often persists after disappearance of the slow-flow phenomenon on angiography. We investigated clinical factors relevant to prolonged ST-segment elevation following RA among 152 patients with stable angina undergoing elective PCI. PCI procedures were divided into two strategies, RA without (primary RA strategy) or with (secondary RA strategy) balloon dilatation before RA. Incidence of prolonged ST-segment elevation after disappearance of slow-flow phenomenon was higher in the 56 patients with primary RA strategy (13%) than in the 96 patients with secondary RA strategy (3%, p = 0.039). Univariate logistic regression analysis showed levels of low-density lipoprotein cholesterol (LDL-C) (odds ratio [OR] 0.95, 95% confidence interval [CI] 0.93-0.99; p = 0.013), levels of triglycerides (OR 0.97, 95%CI 0.94-0.99; p = 0.040), and secondary RA strategy (OR 0.23, 95% CI 0.05-0.85; p = 0.028) were inversely associated with occurrence of prolonged ST-segment elevation following ablation. However, hemodialysis, diabetes mellitus, left-ventricular ejection fraction, lesion length ≥ 20 mm, and burr size did not show significant associations. Multivariate logistic regression analysis modeling revealed that secondary RA strategy was significantly associated with the occurrence of prolonged ST-segment elevation (Model 1: OR 0.24, 95% CI 0.05-0.95, p = 0.042; Model 2: OR 0.17, 95% CI 0.03-0.68, p = 0.018; Model 3: OR 0.21, 95% CI 0.03-0.87, p = 0.041) even after adjusting for levels of LDL-C and triglycerides. Secondary RA strategy may be useful to reduce the occurrence of prolonged ST-segment elevation following RA.

Homocysteine levels in patients with coronary slow flow phenomenon: A meta-analysis.

BACKGROUND: With the development of coronary angiography, more and more attention has been paid to coronary slow flow phenomenon (CSFP). Recent studies have found that the correlation between homocysteine (Hcy) levels and CSFP was contradictory, so we conducted this meta-analysis to investigate the correlation. METHODS: By March 2022, studies that meet the research requirements were identified by searching multiple databases including Embase, Web of Science, and PubMed. We included studies evaluating the correlation between Hcy levels and CSFP. Random or fixed effect meta-analyses were performed according to heterogeneity among included studies. A leave-out method and subgroup analyses were conducted to determine the source of heterogeneity. RESULTS: Thirteen studies involving 625 CSFP and 550 subjects were included. After pooling data from each study, Hcy levels were higher in the CSFP groups (standard mean difference [SMD], 1.45; 95% CI, 0.94 to 1.96, P < .00001) than in the control group. In the meta-analysis, there was significant heterogeneity (I2 = 93%), which was further explored through leave-out method and and subgroup analyses. Specifically, pooling data from studies with a mean thrombolysis in myocardial infarction (TIMI) frame count ≥ 46 (SMD, 1.31; 95% CI, 1.00 to 1.63, P < .00001) resulted in no heterogeneity (0%), indicating that the TIMI frame count ≥ 46 was the source of heterogeneity. CONCLUSIONS: Our study found that elevated Hcy levels are strongly associated with CSFP. More importantly, the association was stronger in CSFP patients with mean TIMI frame count ≥ 46.

An unusual no-reflow phenomenon due to neointimal tissue embolization during drug eluting balloon intervention in stent restenosis: A case report.

Acute coronary syndrome is one of the leading causes of death worldwide. Percutaneous coronary intervention (PCI), along with various devices, have been technically developed to dramatically improve mortality risk in patients with acute myocardial infarction. However, no-reflow phenomenon still remains a problematic complication during a PCI, even in the era of drug eluting stents. There are various hypotheses and mechanisms for no-reflow phenomenon, but none have been confirmed. Treatment for no-reflow phenomenon also depends on various underlying conditions, but have not yet shown effective improvement. We presented a case of no-reflow phenomenon caused by an unusual cause.

Treatment of Slow-Flow After Primary Percutaneous Coronary Intervention With Flow-Mediated Hyperemia: The Randomized RAIN-FLOW Study.

Background ST-segment-elevation myocardial infarction complicated with no reflow after primary percutaneous coronary intervention is associated with adverse outcomes. Although several hyperemic drugs have been shown to improve the Thrombolysis in Myocardial Infarction flow, optimal treatment of no reflow remains unsettled. Saline infusion at 20 mL/min via a dedicated microcatheter causes (flow-mediated) hyperemia. The objective is to compare the efficacy of pharmacologic versus flow-mediated hyperemia in patients with ST-segment-elevation myocardial infarction complicated with no reflow. Methods and Results In the RAIN-FLOW (Treatment of Slow-Flow After Primary Percutaneous Coronary Intervention With Flow-Mediated Hyperemia) study, 67 patients with ST-segment-elevation myocardial infarction and no reflow were randomized to receive either pharmacologic-mediated hyperemia with intracoronary adenosine or nitroprusside (n=30) versus flow-mediated hyperemia (n=37). The angiographic corrected Thrombolysis in Myocardial Infarction frame count and the minimal microcirculatory resistance, as assessed with intracoronary pressure-thermistor wire, dedicated microcatheter, and thermodilution techniques, were compared after study interventions. Both Thrombolysis in Myocardial Infarction frame count(40.2±23.1 versus 39.2±20.7; P=0.858) and minimal microcirculatory resistance (753.6±661.5 versus 993.3±740.8 Wood units; P=0.174) were similar between groups. Thrombolysis in Myocardial Infarction 3 flow was observed in 26.7% versus 27.0% (P=0.899). Flow-mediated hyperemia showed 2 different thermodilution patterns during saline infusion indicative of the severity of the no reflow phenomenon. In-hospital death and nonfatal heart failure were observed in 10.4% and 26.9%, respectively. Conclusions Both treatments showed similar (and limited) efficacy restoring coronary flow. Flow-mediated hyperemia with thermodilution pattern assessment allowed the simultaneous characterization of the no reflow degree and response to hyperemia. No reflow was associated with a high rate of adverse outcomes. Further research is warranted to prevent and to treat no reflow in patients with ST-segment-elevation myocardial infarction. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT04685941.