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.

Prolonged P Wave Peak Time May Be a Sign of LV Diastolic Dysfunction in the Coronary Slow Flow Phenomenon.

Background: The coronary slow flow phenomenon (CSFP) is an atherosclerotic process that causes ischemia at the microvascular level. The CSFP may affect P wave durations, especially P wave peak time (PWPT), by microvascular ischemia, left ventricular diastolic dysfunction, and changes in the left atrial dimension. Therefore, in the present study, we aimed to assess PWPT in the CSFP. Method: One hundred and ninety-five patients were included in this single-center, retrospective study. Ninety patients were enrolled in the CSFP group and 105 patients in the control group. PWPT was defined as the duration between the beginning and peak of the p wave and obtained from the leads Dii and V i. Results: The mean age of the study population was 48.5 ± 9.5, and 108 (55.3%) of the patients were female. We found PWPT was longer in the CSFP group than in the control group. Correlation analysis showed a positive correlation between PWPT in both leads (D II, V i) and left atrial anterior-posterior diameter, mean TIMI frame count (TFC), and E/e. A significant relationship was observed between mean TFC, E/e, EF, heart rate, and PWPT in lead D ii (ß coefficient = 0.33, 95% CI 0.44-1.33, p < 0.001, ß coefficient = 0.23, 95% CI 0.25-1.85, p=0.01, ß coefficient = -0.140, 95% CI -1.04--0.53, p=0.03, and ß coefficient = -0.13, 95% CI -0.29--0.014, p=0.03, respectively) in multivariable linear analysis. Conclusion: In the present study, we found prolonged PWPT in patients with the CSFP and found a relationship between PWPT and mean TFC.

[Intra-aortic balloon pump in patients with myocardial infarction and cardiogenic shock of stages A and B].

This article presents two clinical cases of patients with myocardial infarction and stage A (at risk) and B (beginning) cardiogenic shock who underwent intra-aortic balloon counterpulsation (IABP). In patients with a high risk of classic cardiogenic shock and/or the no-reflow phenomenon, stenting of the infarct-related coronary artery during this type of mechanical circulatory support was performed without complications. Theoretical and practical aspects of using IABP at different stages of cardiogenic shock are discussed.

Prognostic Value of Pre-Infarction Angina Combined with Mean Platelet Volume to Lymphocyte Count Ratio for No-Reflow and Short-Term Mortality in Patients with ST-Segment Elevation Myocardial Infarction Undergoing Percutaneous Coronary Intervention.

BACKGROUND The aim of the present study was to investigate the clinical predictive value of pre-infarction angina (PIA) combined with mean platelet volume to lymphocyte count ratio (MPVLR) for no-reflow phenomenon and short-term mortality in patients with ST-segment elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI). MATERIAL AND METHODS A total of 1009 STEMI patients who had undergone PCI were enrolled and subdivided into 4 groups based on the occurrence of PIA and the presence of MPVLR above or below the cutoff value. Analysis of the predictors of the no-reflow phenomenon and 90-day mortality was conducted. Further, evaluation and comparison of the clinical predictive value of PIA, MPVLR, and their combination were done. RESULTS Both MPVLR (odds ratio [OR]=1.476, 95% confidence interval [CI]: 1.401 to 1.756, P<0.001; hazard ratio [HR]=1.430, 95% CI: 1.287 to 1.643, P<0.001) and PIA (OR=0.905, 95% CI: 0.783 to 0.986, P<0.001; HR=0.878, 95% CI: 0.796 to 0.948, P<0.001) were independent predictors of no-reflow phenomenon and 90-day mortality. Spearman's rank correlation test revealed that MPVLR (r=-0.297, P<0.001), monocyte to lymphocyte count ratio (MLR) (r=-0.211, P<0.001) and neutrophil to lymphocyte count ratio (NLR) (r=-0.389, P<0.001) in peripheral blood were significantly negatively correlated with postoperative left ventricular ejection fraction (LVEF). Upon comparing the area under curve (AUC), the MPVLR combined with PIA achieved better performance in differentiating no-reflow phenomenon (AUC=0.847, 95% CI: 0.821 to 0.874) and 90-day mortality (AUC=0.790, 95% CI: 0.725 to 0.855), than the GRACE score, MPVLR and PIA alone, and had similar performance to all other pairwise combinations of the GRACE score, MPVLR and PIA. CONCLUSIONS High MPVLR and PIA were independent predictors of the no-reflow phenomenon and 90-day mortality in patients with STEMI after PCI. Moreover, Combined application of MPVLR and PIA can effectively predict the occurrence of the no-reflow phenomenon and 90-day mortality.

Early repolarization pattern in the coronary slow flow phenomenon.

BACKGROUND: The coronary slow flow phenomenon (CSFP) is well-documented, and the early repolarization pattern (ERP) has recently been shown to be a risk factor for the development of malignant ventricular arrhythmias. METHODS: Those with true CSFP were included as cases and those with normal angiograms were included as controls. We assessed J-point elevation on surface electrocardiograms (ECGs) and defined ERP as notching or slurring of the terminal portion of the QRS takeoff. RESULTS: We enrolled 115 cases (33 females, 82 males; mean age, 51.9 ± 11.5 years) and 45 controls (13 females, 32 males; mean age, 50.8 ± 11.7 years). ERP was more common among cases than among controls (65% vs. 28%, p = .001). Compared with the controls, cases were more likely to have J-point elevation in the inferior leads (25% vs. 13%, p = .002), in the D1 to aVL leads (22% vs. 15%, p = .001), and in the lateral leads (17.3% vs. 0%), p = .001). Notching was also significantly more common in cases than in controls (26.0% vs. 2.2%, p = .0001). Finally, concave/ascendant ST segment (33.9% vs. 5.2%, p = .006), horizontal/non-ascendant ST segment (14.7% vs. 1.7%, p = .054), and horizontal/non-ascendant ST segment and notching (15.6% vs. 2.2%, p = .012) patterns were more common in cases than in controls. CONCLUSIONS: We report that CSFP is associated with J-wave and slurring ERPs. However, the clinical significance of these changes needs to be clarified.

Cardioprotective Effects of Nicorandil on Coronary Heart Disease Patients Undergoing Elective Percutaneous Coronary Intervention.

BACKGROUND Nicorandil is a nicotinamide ester commonly prescribed for treatment of patients with coronary heart disease (CHD). In the present study, we aimed to explore the cardioprotective effects of nicorandil on CHD patients undergoing elective percutaneous coronary intervention (PCI). MATERIAL AND METHODS One hundred patients with CHD undergoing PCI were randomly divided into a control group (n=48) and a nicorandil group (n=52). Patients in the control group received traditional therapy, and while patients in the nicorandil group received nicorandil before PCI in addition to the traditional therapy. After PCI, all patients underwent coronary angiogram, and TIMI frame count (TFC) was calculated. Plasma levels of cardiac troponin I (cTnI), creatine kinase-MB (CK-MB), myeloperoxidase (MPO), and malondialdehyde (MDA) were determined before and at 6, 18, and 24 h after PCI. Moreover, systolic blood pressure (SBP), mean blood pressure (DBP), heart rate (HR), and left ventricular ejection fractions (LVEF) were recorded before and 3 months after PCI. RESULTS There was a significant difference in the rate of no-reflow (P=0.036) between the 2 groups. The blood frames and levels of cTnI, CK-MB, MPO, and MDA in the nicorandil group were significantly decreased compared to the control group (all P<0.05). Moreover, administration of nicorandil markedly decreased SBP, MBP, and HR, but obviously increased LVEF at 3 months after PCI (P<0.05 or P<0.01). CONCLUSIONS Nicorandil exerts cardioprotective effects on CHD patients undergoing elective PCI by decreasing PCI-related myocardial injury and rate of no-reflow and improvement of LVEF.

Impact of Stress Hyperglycemia on No-Reflow Phenomenon in Patients with ST Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention.

Background: Stress hyperglycemia is a common finding during acute myocardial infarction and associated with poor prognosis. To reduce the occurrence of no-reflow, prognostic factors must be identified before primary percutaneous coronary intervention (PPCI). Our objective was to investigate the impact of stress hyperglycemia in non-diabetic and diabetic patients on no-reflow phenomenon after PPCI. Methods: The study comprised 480 patients with ST elevation myocardial infarction (STEMI) who were managed by PPCI. Patients were classified into two groups according to thrombolysis in myocardial infarction (TIMI) flow grade: Group I (Patients with normal flow, TIMI 3 flow) and Group II (Patients with no-reflow, TIMI 0-2 flow). Patients were analyzed for clinical outcomes including mortality and major adverse cardiac events. Results: Incidence of stress hyperglycemia was 14.8% in non-diabetic patients and 22.2% in diabetic patients; the incidence of no-reflow phenomenon was 13.5% and no-reflow was significantly higher in patients with stress hyperglycemia. Multivariate regression analysis identified the independent predictors of no-reflow phenomenon: stress hyperglycemia OR 3.247 (CI95% 1.656-6.368, P = 0.001), Killip class >1 OR 1.893 (CI95% 1.004-3.570, P = 0.049) and cardiogenic shock OR 3.778 (CI95% 1.458-9.790, P = 0.006). Conclusion: Stress hyperglycemia was associated with higher incidence of no-reflow phenomenon. The independent predictors of no-reflow were stress hyperglycemia, Killip class >1 and cardiogenic shock.

Impaired cerebral circulation in patients with slow coronary flow.

Slow coronary flow (SCF) is characterized by delayed opacification of coronary arteries during coronary angiography and is associated with myocardial perfusion abnormalities, ischemia or myocardial infarction. We hypothesized that SCF could be a part of systemic circulatory abnormalities. Therefore, the present study was conducted to investigate whether cerebral blood flow velocity is altered in patients with SCF. The study included 16 patients suffering from chest pain with angiographically proven SCF and 16 subjects suffering from atypical chest pain with angiographically normal coronary flow. All study subjects were selected among those who undergone routine cardiac catheterization. SCF was defined based on thrombolysis in myocardial infarction frame count that reflects coronary artery flow. Thrombolysis in myocardial infarction frame count was significantly higher in patients with SCF than those with normal coronary flow. The average peak systolic, end diastolic and mean flow velocities of the middle cerebral artery were measured and recorded in both groups by transcranial Doppler ultrasonography. Baseline demographic properties were similar in both groups. Echocardiographic parameters were also similar in patients with SCF and those with normal coronary flow. In contrast, both right and left middle cerebral artery peak systolic, end diastolic and mean flow velocities were significantly lower in patients with SCF than those with normal coronary flow. We conclude that cerebral blood flow velocity is significantly lower in patients with SCF. SCF phenomenon may reflect a part of impaired systemic circulation.

The contribution of intramyocardial hemorrhage to the "no-reflow phenomenon": a study performed by cardiac magnetic resonance.

BACKGROUND: Percutaneous coronary intervention (PCI) in acute myocardial infarction (AMI) is sometimes complicated by microvascular damage and hemorrhage. Hemoglobin degradation products have magnetic susceptibility effects which help in detecting hemorrhagic AMI by T2 -weighted cardiac magnetic resonance (CMR) images. OBJECTIVES: To investigate the possibility to detect intramyocardial hemorrhage after AMI and to assess its contribution to the delayed hypoenhanced core on late gadolinium enhancement (LGE) CMR, a feature traditionally referred to as microvascular obstruction. METHODS: Consecutive patients with AMI who underwent PCI and CMR were investigated. Hypointense zones T2 -weighted images were labelled as "hemorrhagic" AMI. Areas of late hypoenhancement on LGE CMR were considered as regions of persistent microvascular damage (PMD). Only transmural AMI were considered. RESULTS: A total number of 108 transmural AMI patients were eventually enrolled and divided into two groups according to the presence of hypoenhancement on T2 images. Thirty-two patients showed an hypointense stria within the high signal intensity zone on T2 -weighted images; all these patients showed midmural PMD on LGE. Among the remaining 76 patients, only 14 (18.4%) showed PMD in the subendocardial region. The angiographic outcome was worse in patients with hemorrhagic AMI, with a lower prevalence of TIMI 3 (65.6% vs. 96.1%, P = 0.017) and higher prevalence of myocardial blush grade 0 (84.4% vs. 13.2%, P < 0.001) post-PCI. CONCLUSIONS: T2 -weighted CMR in reperfused AMI allows identification of hemorrhage, related to PMD areas on LGE images and to a worse reperfusion profile on angiography. These features open new avenues of investigation for prognostic assessment of reperfused AMI.

No-reflow phenomenon during percutaneous coronary intervention in a patient with polycythemia vera: A case report.

RATIONALE: Acute myocardial infarction is the leading cause of mortality and morbidity in a patient with polycythemia vera (PV). However, the benefit of various percutaneous coronary intervention (PCI) technique on the patient with PV is relatively unexplored. PATIENT CONCERN: A 46-year-old woman presented to the primary hospital complained about new-onset typical chest pain. Echocardiography examination showed inferior ST-elevation myocardial infarction (STEMIs) and increased cardiac markers. Complete blood count showed elevated hemoglobin, white blood cell, and platelet. DIAGNOSIS: Coronary angiography revealed simultaneous total occlusion at proximal right coronary artery (RCA) and also at proximal left anterior descending (LAD) artery. Elevated hemoglobin and hematocrit with JAK2 mutation establish the diagnosis of PV. INTERVENTIONS: We performed multi-vessel primary PCI by using direct stenting in RCA and aspiration thrombectomy in LAD after failed with balloon dilatation and direct stenting method. This procedure resulted in thrombolysis in myocardial infarction (TIMI)-3 flow in both coronary arteries. However, the no-reflow phenomenon occurred in the LAD, followed by ventricular fibrillation. After several attempts of resuscitation, thrombus aspiration, and low-dose intracoronary thrombolysis, the patient was returned to spontaneous circulation. The patient then received dual antiplatelet and cytoreductive therapy. OUTCOMES: The patient clinical condition and laboratory finding were improved, and the patient was discharged on the 7th day after PCI. LESSONS: Cardiologist should be aware of the no-reflow phenomenon risk in the patient with PV and STEMI. Direct stenting, intracoronary thrombectomy, and thrombolysis are preferable instead of balloon dilatation for PCI technique in this patient.

The effect of statins on the no-reflow phenomenon: an observational study in patients with hyperglycemia before primary angioplasty.

BACKGROUND: An association between admission plasma glucose levels and an increased risk of no-reflow has been well documented. Although HMG-CoA reductase inhibitor (statin) therapy can reduce no-reflow, little is known about its effect on no-reflow in patients with hyperglycemia. In the present study, we investigated whether pretreatment with a statin could reduce no-reflow in patients with hyperglycemia, who underwent primary coronary intervention for acute myocardial infarction (AMI). METHODS: A total of 259 consecutive patients who underwent primary angioplasty for a first AMI were studied. Blood glucose and creatinine kinase levels were measured on admission. All patients underwent 2-dimensional echocardiography and electrocardiographic analysis just after admission. No-reflow was defined as a Thrombolysis in Myocardial Infarction (TIMI) flow grade <3. Hyperglycemia was defined as a blood glucose level >or=10 mmol/L. Statin administration prior to admission was determined by detailed interview or information in the medical records. RESULTS: Hyperglycemia was diagnosed in 154 patients on admission. The no-reflow phenomenon was found in 31 of the 154 patients with hyperglycemia. The incidence of no-reflow was significantly greater in patients with hyperglycemia compared with no hyperglycemia. A multivariable logistic regression analysis showed that hyperglycemia on admission was an independent predictor of no-reflow. Among the 154 patients with hyperglycemia, there were no significant differences in baseline clinical characteristics between patients who received statin pretreatment and those who did not; however, hyperlipidemia occurred in a greater number of the patients who did not receive statin pretreatment. The 40 patients with hyperglycemia who received statins before admission had a lower incidence of no-reflow than those who did not receive statin pretreatment (5% and 25.4%; p < 0.05). Multivariable logistic regression analysis revealed that absence of statin pretreatment was a significant predictor of no-reflow in patients with hyperglycemia, along with ejection fraction on admission, initial TIMI 0 flow, number of Q waves, and anterior AMI. CONCLUSION: The results of our study show that pretreatment with statins could attenuate no-reflow after AMI in patients with acute hyperglycemia.

Coronary slow flow phenomenon and microalbuminuria: Is there any relationship?

OBJECTIVE: The pathophysiology of coronary slow flow phenomenon (CSFP) is poorly understood. Evidence suggesting endothelial dysfunction in patients with slow coronary flow (SCF) led to this evaluation of a possible correlation between microalbuminuria (MAU), as an indicator of endothelial dysfunction, and CSFP in order to investigate a mutual pathophysiology. METHODS: In this case-control study, 15786 patients who presented between September 2016 and April 2018 were screened. All patients with CSFP had chest pain and coronary angiography was indicated due to a positive noninvasive test. All cases had a Thrombosis in Myocardial Infarction (TIMI) flow grade of 2 or a corrected TIMI frame count of >27 without any evidence of obstructive coronary artery disease. The patients used as controls had completely normal coronary angiograms. Fasting mid-stream urine samples were analyzed using an immunoturbidimetric assay to determine the albumin-creatinine ratio (ACR) as a surrogate of microalbuminuria (MAU) (ACR: 30-300 mg/g). The prevalence of MAU in the case and control groups was analyzed. RESULTS: A total of 154 individuals with a normal coronary angiogram and 46 patients with SCF were enrolled in the study. The prevalence of MAU was greater in patients with SCF than in the control group (8.7% vs 1.9%, respectively; p=0.048). Even after adjustment for major risk factors, the association between MAU and CSPF remained significant. CONCLUSION: The results of this study indicated that there was a relationship between MAU and CSFP and confirmed that endothelial dysfunction is a contributing factor to CSFP. These findings are of utmost importance due to the prognostic value of MAU for both all-cause and cardiovascular mortality rates.

No-reflow phenomenon in cardiac MRI: diagnosis and clinical implications.

OBJECTIVE: The purposes of this study were to depict the first-pass, delayed contrast enhancement and regional myocardial wall motion abnormalities of no-reflow phenomenon MRI and to review the major mechanisms and significance of this phenomenon in the clinical setting. CONCLUSION: Contrast-enhanced MRI is a useful noninvasive technique for determining the presence of microvascular obstruction. No-reflow phenomenon has important prognostic implications, and knowledge of the physiologic mechanism is important to understanding the distribution patterns of enhancement in correlation with the underlying pathologic process.

A rare case of thromboembolism in a 21-year old female with elevated factor VIII.

In this article we present the history of a previously healthy female adolescent, who was seen at our hospital with abdominal pain. This was the result of a large floating thrombus in the aorta. Widespread embolism occurred, which lead to the loss of a limb and a left hemicolectomy. Although our patient is a smoker, used oral contraceptives and was found to have a heterozygote mutation at the factor V Leiden gene, the most important factor contributing to her thrombophilia is thought to be her significantly elevated factor VIII. We stress an aggressive diagnostic and therapeutic approach in young patients with unknown embolism in order to avoid the grave consequences of delay.

The challenges and impact of microvascular injury in ST-elevation myocardial infarction.

Despite successful restoration of epicardial coronary blood flow, a significant proportion of patients with ST-elevation myocardial infarction suffer from an impairment of the microvascular perfusion - a phenomenon termed no-reflow or microvascular injury (MVI). The underlying pathophysiology is complex and likely multifactorial. It is well established that MVI is associated with worse clinical outcome. Although MVI can be detected during coronary intervention and the post-infarction period, its prevention and treatment strategies remain a major challenge since most results of clinical studies have been disappointing so far. This review provides an overview on the main pathophysiological mechanisms of MVI and its diagnostic approaches. Moreover, it will discuss its clinical consequences and current strategies of prevention and treatment.

The no-reflow phenomenon: State of the art.

Primary percutaneous coronary intervention (PCI) is the best available reperfusion strategy for acute ST-segment elevation myocardial infarction (STEMI), with nearly 95% of occluded coronary vessels being reopened in this setting. Despite re-establishing epicardial coronary vessel patency, primary PCI may fail to restore optimal myocardial reperfusion within the myocardial tissue, a failure at the microvascular level known as no-reflow (NR). NR has been reported to occur in up to 60% of STEMI patients with optimal coronary vessel reperfusion. When it does occur, it significantly attenuates the beneficial effect of reperfusion therapy, leading to poor outcomes. The pathophysiology of NR is complex and incompletely understood. Many phenomena are known to contribute to NR, including leukocyte infiltration, vasoconstriction, activation of inflammatory pathways and cellular oedema. Vascular damage and haemorrhage may also play important roles in the establishment of NR. In this review, we describe the pathophysiological mechanisms of NR and the tools available for diagnosing it. We also describe the microvasculature and the endothelial mechanisms involved in NR, which may provide relevant therapeutic targets for reducing NR and improving the prognosis for patients.

No-Reflow Phenomenon in Central Retinal Artery Occlusion: Incidence, Risk Factors, and Clinical Implications.

PURPOSE: To investigate the incidence and risk factors of the no-reflow phenomenon in central retinal artery occlusion (CRAO) patients and to determine its effects on visual and anatomic outcomes. METHODS: In 102 eyes with CRAO in which arterial recanalization was obtained within 1 week from baseline, fluorescein angiography images obtained at baseline and 1 week were retrospectively reviewed. The no-reflow phenomenon in the retina was defined as macular capillary nonperfusion following arterial recanalization on fluorescein angiographs. We investigated the incidence and risk factors for the no-reflow phenomenon and compared the anatomical and visual outcomes between eyes with and without the phenomenon. RESULTS: Among the 102 CRAO eyes with arterial recanalization, 39 exhibited the no-reflow phenomenon, resulting in an incidence of 38.2%. The incidence among the eyes with treatment-induced and spontaneous recanalization was 43.4% and 15.8%, respectively, and it increased with the CRAO stage. CRAO stage and increased central macular thickness were risk factors for the phenomenon, with an odds ratio of 4.47 [95% confidence interval (CI), 1.19-16.8; P = 0.027] and 1.69 (95% CI, 1.12-2.55; P = 0.012) per 100-µm increase, respectively. The visual outcome was significantly poorer and retinal atrophy and photoreceptor disruption was greater in eyes with the no-reflow phenomenon than in those without. CONCLUSIONS: The no-reflow phenomenon may occur after arterial recanalization in approximately one-third of CRAO patients and can affect anatomical and visual outcomes. This phenomenon may provide an additional explanation regarding the permanent retinal damage and vision loss in eyes with CRAO.

Plasma factor XI and XII activity in patients with slow coronary flow.

The exact pathophysiology of slow coronary flow (SCF) phenomenon, characterized by delayed opacification of coronary arteries during coronary angiography, is still unknown, although endothelial dysfunction, inflammation, vasomotor disorders and atherosclerosis are shown. The present study was conducted to investigate whether there is a coagulation pathway abnormality in patients with SCF measuring plasma factor XI and XII activity. The study included 55 patients with angiographically proven SCF (group I) and 40 individuals with normal coronary flow (NCF, group II). Baseline demographic properties were similar in both groups. Echocardiographic parameters were also similar in patients with SCF and NCF. Factor XI activity was significantly higher in group I when compared with group II. Factor XII activity was also significantly higher in group I when compared with group II (108.9 ±â€Š19 vs. 98.8 ±â€Š20, P = 0.018 and 131.2 ±â€Š17 vs. 119.1 ±â€Š16, P = 0.001, respectively). We conclude that SCF phenomenon appears to be associated with enhanced procoagulant state, which may support the role of inflammation and atherosclerosis in the pathogenesis of this phenomenon.

Assessment of the relationship between a narrow fragmented QRS complex and coronary slow flow.

BACKGROUND: The coronary slow flow (CSF) phenomenon is a delayed antegrade progression of contrast agent to the distal branch of a coronary artery in the absence of obstructive coronary artery disease (CAD). A narrow fragmented QRS (fQRS) has been reported as a significant predictor of sudden cardiac death in patients with idiopathic dilated cardiomyopathy. The present study aimed to investigate the relationship between a narrow fQRS on the admission electrocardiogram (ECG) and CSF on coronary angiography. METHODS: This study included 165 consecutive patients (112 CSF, 53 controls) who underwent first-time diagnostic conventional coronary angiography for suspected CAD. Coronary flow was quantified by thrombolysis in myocardial infarction (TIMI) frame count (TFC). The patients were divided into two groups according to the presence or absence of a narrow fQRS complex on the admission ECG. RESULTS: Forty four patients were in the fQRS group (mean age, 52.97 ± 3.13 years). There was no difference between the two groups with respect to age, gender, body mass index, family history, hyperlipidemia, hypertension, or diabetes mellitus. The extent of CSF was significantly greater in the fQRS group compared to the non-fragmented group (p < 0.001). A significant correlation was also found between mean TFC values and fQRS (p < 0.001). On multivariate analysis, only CSF (p = 0.03) was a significant independent predictor for narrow fQRS, after adjustment for other parameters. CONCLUSIONS: The narrow fQRS is a simple, inexpensive, and readily available noninvasive ECG parameter that may be a new potential indicator of myocardial damage in patients with CSF.

The preventive effect of garlicin on a porcine model of myocardial infarction reperfusion no-reflow.

OBJECTIVE: To evaluate whether garlicin can prevent reperfusion no-reflow in a catheter-based porcine model of acute myocardial infarction (AMI). METHODS: Twenty-two male Chinese mini swines were randomized into 3 groups: sham-operation group (n=6), control group (n=8), and garlicin group (n=8). The distal part of left anterior descending coronary artery (LAD) in swines of the latter two groups was completely occluded by dilated balloon for 2 h and a successful AMI model was confirmed by coronary angiography (CAG) and electrocardiograph (ECG), which was then reperfused for 3 h. In the sham-operation group, balloon was placed in LAD without dilatation. Garlicin at a dosage of 1.88 mg/kg was injected 10 min before LAD occlusion until reperfusion for 1 h in the garlicin group. To assess serial cardiac function, hemodynamic data were examined by catheter method before AMI, 2 h after occlusion and 1, 2, and 3 h after reperfusion. Myocardial contrast echocardiography (MCE) and double staining with Evans blue and thioflavin-S were performed to evaluate myocardial no-reflow area (NRA) and risk area (RA). RESULTS: Left ventricular systolic pressure and left ventricular end-diastolic pressure significantly improved in the garlicin group after reperfusion compared with the control group P<0.05) and 2 h after AMI (P<0.05). MCE showed garlicin decreased reperfusion NRA after AMI compared with the control group (P <0.05). In double staining, NRA/RA in the garlicin group was 18.78%, significantly lower than that of the control group (49.84%, P<0.01). CONCLUSIONS: Garlicin has a preventive effect on the porcine model of myocardial infarction reperfusion no-reflow by improving hemodynamics and decreasing NRA.