Larger Myocardial Infarction Size Research Articles

Brown Adipose Tissue and BMP3b Decrease Injury in Cardiac Ischemia-Reperfusion.

Despite advances in treatment, myocardial infarction (MI) is a leading cause of heart failure and death worldwide, with both ischemia and reperfusion (I/R) causing cardiac injury. A previous study using a mouse model of nonreperfused MI showed activation of brown adipose tissue (BAT). Recent studies showed that molecules secreted by BAT target the heart. We investigated whether BAT attenuates cardiac injury in I/R and sought to identify potential cardioprotective proteins secreted by BAT. Myocardial I/R surgery with or without BAT transplantation was performed in wild-type (WT) mice and in mice with impaired BAT function (uncoupling protein 1 [Ucp1]-deficient mice). To identify potential cardioprotective factors produced by BAT, RNA-seq (RNA sequencing) was performed in BAT from WT and Ucp1-/- mice. Subsequently, myocardial I/R surgery with or without BAT transplantation was performed in Bmp3b (bone morphogenetic protein 3b)-deficient mice, and WT mice subjected to myocardial I/R were treated using BMP3b. Dysfunction of BAT in mice was associated with larger MI size after I/R; conversely, augmenting BAT by transplantation decreased MI size. We identified Bmp3b as a protein secreted by BAT after I/R. Compared with WT mice, Bmp3b-deficient mice developed larger MIs. Increasing functional BAT by transplanting BAT from WT mice to Bmp3b-deficient mice reduced I/R injury whereas transplanting BAT from Bmp3b-deficient mice did not. Treatment of WT mice with BMP3b before reperfusion decreased MI size. The cardioprotective effect of BMP3b was mediated through SMAD1/5/8. In humans, the plasma level of BMP3b increased after MI and was positively correlated with the extent of cardiac injury. The results of this study suggest a cardioprotective role of BAT and BMP3b, a protein secreted by BAT, in a model of I/R injury. Interventions increasing BMP3b levels or targeting Smad 1/5 may represent novel therapeutic approaches to decrease myocardial damage in I/R injury.

Endothelial Transient Receptor Potential Canonical Channel Regulates Angiogenesis and Promotes Recovery After Myocardial Infarction.

BackgroundTransient receptor potential canonical (TRPC) channels play a role in angiogenesis. However, the involvement of TRPC1 in myocardial infarction (MI) remains unclear. The present study was aimed at investigating whether TRPC1 can improve the recovery of cardiac function via prompting angiogenesis following MI.Methods and ResultsIn vitro, coronary artery endothelial cells from floxed TRPC1 mice and endothelial cell‐specific TRPC1 channel knockout mice were cultured to access EC angiogenesis. Both EC tube formation and migration were significantly suppressed in mouse coronary artery endothelial cells from endothelial cell‐specific TRPC1 channel knockout mice. In vivo, coronary artery endothelial cells from floxed TRPC1 and endothelial cell‐specific TRPC1 channel knockout mice were subjected to MI, then echocardiography, triphenyltetrazolium chloride staining and immunofluorescence were performed to assess cardiac repair on day 28. Endothelial cell‐specific TRPC1 channel knockout mice had higher ejection fraction change, larger myocardial infarct size, and reduced capillary density in the infarct area compared with coronary artery endothelial cells from floxed TRPC1 mice. Furthermore, we found underlying regulation by HIF‐1α (hypoxic inducible factor‐1α) and MEK‐ERK (mitogen‐activated protein kinase/extracellular signal‐regulated kinase) that could be the mechanism for the angiogenetic action of TRPC1. Significantly, treatment with dimethyloxaloylglycine, an activator of HIF‐1α, induced cardiac improvement via the HIF‐1α‐TRPC1‐MEK/ERK pathway in MI mice.ConclusionsOur study demonstrated TRPC1 improves cardiac function after MI by increasing angiogenesis via the upstream regulator HIF‐1α and downstream MEK/ERK, and dimethyloxaloylglycine treatment has protective effect on MI through the HIF‐1α‐TRPC1‐MEK/ERK pathway.

Activation of transient receptor potential vanilloid 4 exacerbates myocardial ischemia-reperfusion injury via JNK-CaMKII phosphorylation pathway in isolated mice hearts

Previous studies, including our own, have demonstrated that transient receptor potential vanilloid 4 (TRPV4) is involved in myocardial ischemia-reperfusion (IR) injury, yet its underlying molecular mechanism remains unclear. In this study, we isolated mice hearts for a Langendorff perfusion test and used HL-1 myocytes for in vitro assessments. We first confirmed that TRPV4 agonist (GSK101) enhanced myocardial IR injury, as demonstrated by the reduced recovery of cardiac function, larger myocardial infarct size, and more apoptotic cells. We also found that GSK101 could further increase the phosphorylation of JNK and CaMKII in isolated hearts during IR. Notably, GSK101 dose-dependently evoked the phosphorylation of JNK and CaMKII in isolated normal hearts. All above GSK101-induced effects could be significantly blocked by the pharmacological inhibition or genetic ablation of TRPV4. More importantly, JNK inhibition (with SP600125) or CaMKII inhibition (with KN93 or in transgenic AC3-I mice) could prevent GSK101-induced myocardial injury during IR. In HL-1 myocytes, GSK101 triggered Ca2+ influx and evoked the phosphorylation of JNK and CaMKII but these effects were abolished by removing extracellular Ca2+ or in the presence of a TRPV4 antagonist. Finally, we showed that in HL-1 myocytes and isolated hearts during IR, JNK inhibition significantly inhibited the phosphorylation of CaMKII induced by GSK101 but CaMKII inhibition had no effect on JNK activation induced by GSK101. Our data suggest that TRPV4 activation exacerbates myocardial IR injury via the JNK-CaMKII phosphorylation pathway.

Association of Circulating Ketone Bodies With Functional Outcomes After ST-Segment Elevation Myocardial Infarction

BackgroundCirculating ketone bodies (KBs) are increased in patients with heart failure (HF), corresponding with increased cardiac KB metabolism and HF severity. However, the role of circulating KBs in ischemia/reperfusion remains unknown. ObjectivesThis study sought to investigate longitudinal changes of KBs and their associations with functional outcomes in patients presenting with ST-segment elevation myocardial infarction (STEMI). MethodsKBs were measured in 369 participants from a randomized trial on early metformin therapy after STEMI. Nonfasting plasma concentrations of KBs (β-hydroxybutyrate, acetoacetate, and acetone) were measured by nuclear magnetic resonance spectroscopy at presentation, at 24 hours, and after 4 months. Myocardial infarct size and left ventricular ejection fraction (LVEF) were determined by cardiac magnetic resonance imaging at 4 months. Associations of circulating KBs with infarct size and LVEF were determined using multivariable linear regression analyses. ResultsCirculating KBs were high at presentation with STEMI (median total KBs: 520 μmol/L; interquartile range [IQR]: 315-997 μmol/L). At 24 hours after reperfusion, KBs were still high compared with levels at 4-month follow-up (206 μmol/L [IQR: 174-246] vs 166 μmol/L [IQR: 143-201], respectively; P < 0.001). Increased KB concentrations at 24 hours were independently associated with larger myocardial infarct size (total KBs, per 100 μmol/L: β = 1.56; 95% confidence interval: 0.29-2.83; P = 0.016) and lower LVEF (β = −1.78; 95% CI: (−3.17 to −0.39; P = 0.012). ConclusionsCirculating KBs are increased in patients presenting with STEMI. Higher KBs at 24 hours are associated with functional outcomes after STEMI, which suggests a potential role for ketone metabolism in response to myocardial ischemia. (Metabolic Modulation With Metformin to Reduce Heart Failure After Acute Myocardial Infarction: Glycometabolic Intervention as Adjunct to Primary Coronary Intervention in ST Elevation Myocardial Infarction (GIPS-III): a Randomized Controlled Trial; NCT01217307)

Abstract 16538: Circulating Ketone Levels are Associated With Myocardial Infarct Size and Left Ventricular Function in Patients Presenting With St-Elevation Myocardial Infarction

Background: Circulating ketone bodies (KB) are increased in patients with heart failure, corresponding with increased utilization of KB as a cardiac fuel. Whether circulating KB are increased in patients presenting with ST-elevation myocardial infarction (STEMI) and whether this is associated with infarct size is unknown. Methods: KB were measured in 379 non-diabetic participants of the Glycometabolic Intervention as Adjunct to Primary Percutaneous Coronary Intervention in ST-Segment Elevation Myocardial Infarction (GIPS) III trial (Clinicaltrial.gov Identifier: NCT01217307). Non-fasting plasma concentrations of the KB beta-hydroxybutyrate, acetoacetate, acetone were measured at presentation, 24 hours and 4 months after STEMI presentation using nuclear magnetic resonance spectroscopy. Associations of circulating KB with myocardial infarct size and left ventricular ejection fraction (both detected with MRI at 4 months after STEMI) were determined using multivariable linear regression analyses. Results: Circulating KB were higher at baseline (total KB 520 [315-997](median [IQR], μmol/L), compared to 206 [174-246] at 24 hours and 166 [143-201] at 4 months ( P &lt;0.001 for all)). KB at 24 hours were positively associated with enzymatic infarct size, HbA1C and beta-blocker use. KB at 24 hours were independently associated with MRI outcomes at 4 months. Higher KB was associated with larger myocardial infarct size (total KB: standardized β=0.17, 95%-confidence interval (CI) (0.04-0.31), P =0.012) and lower ejection fraction (standardized β=-0.15, 95%-CI (-0.29- -0.009), P =0.037). Conclusion: Circulating KB are increased in patients with STEMI and are independently associated with myocardial infarct size and left ventricular function after 4 months of follow-up. The increase in circulating KB may reflect maladaptive changes of myocardial metabolism during the acute phase.

ST-Segment-Elevation Myocardial Infarction Care and COVID-19: The Value Proposition of Fibrinolytic Therapy and the Pharmacoinvasive Strategy.

ST-Segment-Elevation Myocardial Infarction Care and COVID-19: The Value Proposition of Fibrinolytic Therapy and the Pharmacoinvasive Strategy.

Overexpression of farnesyl pyrophosphate synthase increases myocardial ischemia/reperfusion injury in mice

Farnesyl pyrophosphate synthase (FPPS) is a vital enzyme in the mevalonate pathway. Our previous study has indicated that overexpression of FPPS increases hypoxia/reoxygenation (HR) injury in Heart-derived H9c2 Cells. Hence, we designed this experiment to further investigate the effect of FPPS on myocardial ischemia/reperfusion (MIR) injury using a transgenic (Tg) model, and explore the relevant mechanisms. The results showed that when mouse hearts were subjected to ex vivo I/R, Tg mice have a higher CK and LDH, a larger myocardial infarct size and lower heart function recovery. These phenomena are associated with the increased Rac1 activity and ROS generation. These findings point to that FPPS might be a potential target in preventing MIR in vivo.

D-Dimer Levels Predict Myocardial Injury in ST-Segment Elevation Myocardial Infarction: A Cardiac Magnetic Resonance Imaging Study.

ObjectivesElevated D-dimer levels on admission predict prognosis in patients undergoing primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI), but the association of D-dimer levels with structural markers of myocardial injury in these patients is unknown.MethodsWe performed cardiac magnetic resonance (CMR) imaging in 208 patients treated with primary PCI for STEMI. CMR was performed a median of 3 days after the index procedure. Of the 208 patients studied, 75 patients had D-dimer levels above the normal range on admission (>0.5 μg/mL; high D-dimer group) while 133 had normal levels (≤0.5 μg/mL; low D-dimer group). The primary outcome was myocardial infarct size assessed by CMR. Secondary outcomes included area at risk (AAR), microvascular obstruction (MVO) area, and myocardial salvage index (MSI).ResultsIn CMR analysis, myocardial infarct size was larger in the high D-dimer group than in the low D-dimer group (22.3% [16.2–30.5] versus 18.8% [10.7–26.7]; p = 0.02). Compared to the low D-dimer group, the high D-dimer group also had a larger AAR (38.1% [31.7–46.9] versus 35.8% [24.2–45.3]; p = 0.04) and a smaller MSI (37.7 [28.2–46.9] versus 47.1 [33.2–57.0]; p = 0.01). In multivariate analysis, high D-dimer levels were significantly associated with larger myocardial infarct (OR 2.59; 95% CI 1.37–4.87; p<0.01) and lower MSI (OR 2.62; 95% CI 1.44–4.78; p<0.01).ConclusionsIn STEMI patients undergoing primary PCI, high D-dimer levels on admission were associated with a larger myocardial infarct size, a greater extent of AAR, and lower MSI, as assessed by CMR data. Elevated initial D-dimer level may be a marker of advanced myocardial injury in patients treated with primary PCI for STEMI.

Effects of late exercise on cardiac remodeling and myocardial calcium handling proteins in rats with moderate and large size myocardial infarction

BackgroundPhysical exercise attenuates myocardial infarction (MI)-induced cardiac remodeling. However, it is unsettled whether late exercise modulates post-infarction cardiac remodeling differentially according to infarct size. We investigated the effects of exercise started at late stage heart failure on cardiac remodeling in rats with moderate and large sized MI. MethodsThree months after MI, rats were assigned into sedentary and exercise groups. Exercise rats underwent treadmill for three months. After assessing infarct size by histological analysis, rats were subdivided into four groups: moderate MI sedentary (Mod MI-Sed; n=7), Mod MI exercised (Mod MI-Ex; n=7), Large MI-Sed (n=11), and Large MI-Ex (n=10). ResultsBefore exercise, MI-induced cardiac changes were demonstrated by comparing results to a Sham group; alterations were more intense in rats with large than moderate MI size. Systolic function, evaluated by echocardiogram using the variation in LV fractional area change between after and before exercise, was improved in exercise than sedentary groups. Calsequestrin expression increased in exercised compared to sedentary groups. L-type calcium channel was higher in Mod MI-Ex than Mod MI-Sed. SERCA2a, phospholamban, and Na+/Ca2+ exchanger expression did not differ between groups. ConclusionLate exercise improves systolic function and modulates intracellular calcium signaling proteins in rats with moderate and large MI.

Abstract 17966: Circadian Variation of Intracoronary Thrombus Aspiration Efficacy in Patients With St-segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Introduction: The clinical benefit of intracoronary thrombus aspiration (TA) during primary percutaneous coronary intervention (PCI) in patients with STEMI remains controversial. Different studies have suggested a circadian variation of myocardial infarction size (IS) among patients with STEMI depending on the time of the day at symptom onset. Hypothesis: Clinical efficacy of manual TA varies according to circadian rhythms. Methods: We analyzed data from a large, nationwide, prospective, multicenter registry of patients admitted with ACS in Switzerland (AMIS). Patients undergoing primary PCI for STEMI with (TA+) or without (TA-) manual TA within 12 hours of symptom onset were included. We divided 24 hours into 4 time groups based on the time of symptom onset: group 1 (00:00-05:59), group 2 (06:00-11:59), group 3 (12:00-17:59) and group 4 (18:00-23:59). The primary endpoint was in-hospital all-cause mortality. Results: Between 2008 and 2014, a total of 3,648 patients (TA+, n=1,800; TA-, n=1,848) were included. In-hospital death of any cause occurred in 3.8% of the patients in the TA+ group, as compared with 3.7% in the TA- group (p=0.44). In-hospital mortality was not statistically different between the 4 time groups in TA+ and TA- patients (2.1%, 4.6%, 2.9% and 5.1% respectively in TA+ group, p=0.082 and 3.1%, 3.0%, 5.6% and 2.9% respectively in TA- group, p=0.098). We observed a circadian variation of myocardial IS in patients undergoing TA with larger myocardial IS occurring during the night period (group 1: 2,833±2,304 U/l; group 2: 2,449±2,336 U/l; group 3: 2,542±2,114 U/l; group 4: 2,995±2,424 U/l, p=0.001). Of note, there was a statistically significant net benefit of manual TA in terms of myocardial salvage in patients with symptom onset between 06:00 and 18:00 (groups 1 vs. 2: p&lt;0.001; groups 1 vs. 3: p&lt;0.05; groups 4 vs. 2: p&lt;0.001; groups 4 vs. 3: p &lt;0.05). Conclusion: In a real-world registry of patients with STEMI, intracoronary TA during primary PCI was not associated with improved in-hospital all-cause mortality, independently of the time of symptom onset. However, our results suggest a circadian variation of the efficacy of manual TA with a significant reduction of myocardial IS in patients with symptom onset between 06:00 and 18:00.

Impact of glycemic variability in patients with ST-elevated myocardial infarction

Acute hyperglycemic state at admission had been demonstrated to be associated with an increased risk of mortality and larger myocardial infarct size in patients with ST-elevation myocardial infarction (STEMI) [1,2]. Most studies have defined the acute hyperglycemic state as a glucose levels≥180mg/dl at admission [1–3]. However, there still remains unclear whether glycemic variability during the days after admission has any prognostic significance in STEMI patients. A newly developed continuous glucose monitoring (CGM) system can obtain accurate readings of glucose levels and fluctuations after PCI.

Targeted deletion of regulatory T cells attenuates the protective effects of myocardial ischemic preconditioning in rats

Background. Myocardial ischemia-reperfusion injury (IRI) is associated with activation of the innate immune system and the resultant inflammatory response. Myocardial ischemic preconditioning (IPC) is the most powerful endogenous protective mechanism against myocardial IRI, probably via the role of anti-inflammation. Regulatory T cells (Tregs), which are characterized by the expression of the forkhead/winged-helix transcription factor FoxP3, play an important role in the negative modulation of immune responses. We tested the hypothesis that Tregs may contribute to the protective effect of myocardial IPC through anti-inflammatory mechanisms. Methods and results. The left anterior descending coronary arteries of rats were occluded for a 30-min ischemia, followed by a 48-h reperfusion. Myocardial IPC was induced by 4 cycles of 5-min ischemia and 5-min reperfusion. Ischemia was achieved by ligation of the left anterior descending coronary artery (LAD), and reperfusion was initiated by releasing the ligature. Rats were injected with a Treg cell-depleting antibody or normal rat immunoglobulin (IgG), after IPC. The accumulation of Tregs was observed at indexed time points following IPC. The protein expression of FoxP3 significantly increased in the myocardium after IPC, and peaked at day-2. Treatment of preconditioned rats with the Treg cell-depleting antibody demonstrated less protein expression of FoxP3 (p < 0.001), more infiltration of inflammatory cells in the myocardium (p < 0.01), and larger myocardial infarct size (p < 0.001), compared with the IgG injection group. Conclusion. Cardioprotection by IPC is associated with Tregs.

Time of symptom onset and value of myocardial blush and infarct size on prognosis in patients with ST-elevation myocardial infarction

In patients with ST-segment elevation myocardial infarction (STEMI), the time of onset of ischemia has been associated with myocardial infarction (MI) size. Myocardial blush grade (MBG) reflects myocardial response to ischemia/reperfusion injury, which may differ according to time of the day. The aim of our study was to explore the 24-hour variation in MBG and MI size in relation to outcomes in STEMI patients. A retrospective multicenter analysis of 6970 STEMI patients was performed. Time of onset of STEMI was divided into four 6-hour periods. STEMI patients have a significant 24-hour pattern in onset of symptoms, with peak onset around 09:00 hour. Ischemic time was longest and MI size, estimated by peak creatine kinase concentration, was largest in patients with STEMI onset between 00:00 and 06:00 hours. Both MBG and MI size were independently associated with mortality. Time of onset of STEMI was not independently associated with mortality when corrected for baseline and procedural factors. Interestingly, patients presenting with low MBG between 00:00 and 06:00 hours had a better prognosis compared to other groups. In conclusion, patients with symptom onset between 00:00 and 06:00 hours have longer ischemic time and consequently larger MI size. However, this does not translate into a higher mortality in this group. In addition, patients with failed reperfusion presenting in the early morning hours have better prognosis, suggesting a 24-hour pattern in myocardial protection.

Three‐Dimensional Speckle Tracking Echocardiography for the Evaluation of the Infarct Size and Segmental Transmural Involvement in Patients with Acute Myocardial Infarction

To compare parameters between three-dimensional speckle tracking echocardiography (3DSTE) and delayed enhancement magnetic resonance imaging (DE-MRI) for estimating myocardial infarct size, peak systolic strain, and transmural involvement of infarct segments in patients with acute myocardial infarction (AMI). Delayed enhancement MRI was conducted to determine myocardial infarction (MI) position, size, and transmural involvement in 26 patients with AMI. 3DSTE was conducted to measure global peak systolic strain in the left ventricle and to estimate longitudinal, circumferential, and radial peak systolic strain in papillary muscle segments. Conventional echocardiography was used to calculate the wall-motion score index (WMSI) and left ventricular ejection fraction (LVEF). Left ventricular strain parameters and LVEF were statistically significantly lower in patients with large-size MI than in those with small-size MI. Global longitudinal strain (GLS) and global circumferential strain (GCS) were significantly lower in patients with moderate-size MIs than in those with small-size MIs. All parameters except ejection fraction (EF) were lower in patients with large-size MI compared with those with moderate-size MI (P<0.05). Pearson analysis revealed that left ventricular GCS, GLS, GRS, WMSI, and LVEF of AMI patients correlated with the myocardial infarct area (MIA) measured by MRI (r=0.86, 0.81, -0.71, 0.64, and -0.66, respectively; all P-values <0.01). Transmural infarct segments exhibited significantly lower longitudinal, circumferential, and radial strains than normal segments (P<0.05). These findings indicate that 3DSTE can distinguish between MIs of different infarct sizes, and may provide an indirect means for the accurate determination of transmural involvement in infarct segments.

Prophylactic amiodarone and lidocaine improve survival in an ovine model of large size myocardial infarction

BackgroundLarge animal models serve as a critical link in the translation of basic science to clinical practice. However, large animal models of myocardial infarction (MI), especially large size MI, have been associated with high mortality because of arrhythmia. The prophylactic effect of amiodarone and lidocaine were retrospectively reviewed in our ovine MI model. Materials and methodsA total of 114 Dorset hybrid sheep with 25%–30% MI were included in the present study. The sheep were prophylactically treated with amiodarone plus lidocaine before ligation of the four to six coronary artery branches supplying the apex of the heart (arrhythmia prevention [AP] group, n = 45) and with epinephrine (shock prevention [SP] group, n = 49), respectively. The sheep without prophylactic treatment (no prevention [NP] group, n = 20) were used as the control group. The incidence of arrhythmia requiring treatment, mortality due to arrhythmia, hemodynamics, and arterial blood gas values during surgery were analyzed in these three groups. ResultsNo significant difference was found in infarct size among the three groups. The incidence of arrhythmia requiring treatment was significantly decreased in the AP group compared with that in the NP or SP groups (4.4% for AP versus 35% for NP and 45% for SP groups; P < 0.05). The mortality due to lethal arrhythmia was 2.2% in the AP group, significantly lower than that in the NP group (15%) or SP group (18.4%). Other than the heart rate, no significant differences were found in the hemodynamic data between the AP and NP groups. Metabolic acidosis was not observed in any group, as indicated by the pH and lactate values. ConclusionsProphylactic amiodarone plus lidocaine decreased the mortality due to lethal arrhythmia after acute MI in our sheep model without significant negative effects on the hemodynamics. However, epinephrine improved the hemodynamics but also increased the mortality due to lethal arrhythmia. Thus, prophylactic amiodarone plus lidocaine is recommended to improve the stability in a large MI animal model.

A Comparison Between Imidapril and Ramipril on Attenuation of Ventricular Remodeling After Myocardial Infarction

Angiotensin converting enzyme inhibitors have been used clinically to prevent myocardial infarction (MI). The angiotensin converting enzyme inhibitors attenuated ventricular remodeling and improved cardiac function by inhibition of matrix metalloproteinases after MI. Although the effect is thought to be a class effect, there are significant differences among the drugs. The aim of this study was to compare the effects of imidapril and ramipril on ventricular remodeling after MI. The middle portion of left anterior descending artery was ligated to induce a moderate size MI in rats (moderate MI group). The proximal portion of the artery was ligated to induce a large size MI (large MI group). The animals were assigned to subgroups in moderate MI group and large MI group: (1) nontreated group, (2) ramipril group (1 mg/kg daily), and (3) imidapril group (1 mg/kg daily). All rats were killed on day 28 after the MI operation. Although the nontreated MI group showed impaired ventricular contraction and severe fibrosis, imidapril significantly negated ischemia-induced changes. Imidapril had a superior effect for preventing ventricular remodeling characterized by fibrosis and collagen accumulation in left ventricle compared with ramipril in the moderate and large MI groups, even though the dosage used in this study was too small to reduce systemic blood pressure. Imidapril can be used as a substitute for ramipril to prevent ventricular remodeling after MI.

Metabolic syndrome influencing infarct size and heart failure in patients with acute coronary syndrome — does gender matter?

Metabolic syndrome (MetS) is the occurrence of diabetes mellitus/glucose intolerance, arterial hypertension, central obesity, dyslipidemia, and microalbuminuria in the same patient (definition by WHO). Presence of metabolic syndrome is associated with larger myocardial infarction size and complications following acute myocardial infarction. Two hundred and thirty patients with acute coronary syndromes were analyzed. Those with MetS (n=141) included patients with diabetes mellitus/glucose intolerance and at least two of the following criteria: hypertension, hypertriglyceridemia/low HDL cholesterol, android obesity/body mass index (BMI) ≥ 30, or microalbuminuria. Control group did not meet criteria for MetS. Presence of heart failure was assigned according to Killip classification. The MetS group had larger myocardial infarction size determined by peak creatine-kinase (CK) (1484±1354 vs. 981±890, p = 0.003) and CK MB (141±117 vs. 95±78, p = 0.002). While in non-MetS group males had larger myocardial infarction than females, in MetS group females had larger myocardial infarction than males. Cardiac failure occurred more in MetS group of patients, again was more prominent in females. Occurrence of metabolic syndrome in acute coronary syndrome patients predisposes to larger myocardial infarction size, more on the account of female patients having MetS. MetS, again particularly in females, predisposes to higher chance of having heart failure during acute coronary syndrome. Recognizing the female group with MetS as of higher risk for large myocardial infarction and heart failure leads us to pay special attention on this patient population.

Left ventricular filling patterns in patients with previous myocardial infarction measured by conventional cine cardiac magnetic resonance

To explore left ventricular filling patterns in patients with a history of previous myocardial infarction (MI) using time-volume curves obtained from conventional cine-cardiac magnetic resonance (CMR) examinations. Consecutive patients with a history of previous MI who were referred for CMR evaluation constituted the study population, and a consecutive cohort of sex and age-matched patients with a normal CMR constituted the control group. The following CMR diastolic parameters were evaluated: peak filling rate (PFR), time to PFR (tPFR), normalised PFR adjusted for diastolic volume at PFR (nPFR), and percent RR interval between end systole and PFR. Fifty patients were included, 25 with a history of previous MI and 25 control. The mean age was 59.6 ± 13.9 years and 27 (54%) were male. Within the control group, age was significantly related to PFR (r = -0.53, p = 0.007), whereas among patients with previous MI age was not related to PFR (r = -0.16, p = 0.44). PFR (252.4 ± 96.7 ml/s vs. 316.0 ± 126.4 ml/s, p = 0.05) and nPFR (1.6 ± 1.2 vs. 3.3 ± 1.5, p < 0.001) were significantly lower in patients with previous MI, whereas no significant differences were detected regarding tPFR (143.0 ± 67.5 ms vs. 176.2 ± 83.9 ms, p = 0.13) and % RR to PFR (18.1 ± 9.7% vs. 20.6 ± 12.2%, p = 0.44). MI size was related to LV ejection fraction (r = -0.76, p < 0.001), PFR (r = -0.40, p = 0.004), nPFR (r = -0.52, p < 0.001) and left atrium area (r = 0.40, p = 0.004). Patients at the lowest PFR quartile (<200 ml/s) showed a larger MI size (Q1 26.5 ± 25.5%, Q2 15.5 ± 20.9%, Q3 6.3 ± 12.4%, Q4 8.8 ± 14.1%, p = 0.04). At multivariate analysis, MI size was the only independent predictor of the lowest PFR (p = 0.017). Infarct size has an impact on LV filling profiles, as assessed by conventional cine CMR without additional specific pulse sequences.

Relationship between location and size of myocardial infarction and their reciprocal influences on post-infarction left ventricular remodeling

Background Patients with anterior MI experience worse LV remodeling and dysfunction than non-anterior MI patients. It remains unclear whether this difference is due to larger MI size or whether infarct location plays a role beyond MI size. Study aim To assess the relationship between myocardial infarction (MI) location and size and their reciprocal influences on post-infarction left ventricular (LV) remodeling. Methods A cohort of 260 reperfused ST-segment elevation MI patients was studied with cardiovascular magnetic resonance (CMR) at 1-week (baseline) and 4-month (followup). Area at risk (AAR) and MI size were quantified by T2-weighted and late gadolinium enhancement imaging, respectively. Adverse LV remodeling was defined as increase in LV end-systolic volume ≥15% at follow-up. Results One-hundred twenty-seven(49%) patients had anterior MI and 133(51%) patients had non-anterior MI. Although the degree of myocardial salvage was similar between groups (p=0.74), anterior MI patients had larger AAR and MI size than non-anterior MI patients yielding worse regional and global LV function at baseline and follow-up. At univariable analysis, anterior MI was associated with increased risk of adverse LV remodeling (p=0.017) and lower LV ejection-fraction at follow-up (p=0.001), but not when accounted for baseline MI size. Accordingly, at multivariable analysis baseline MI size but not its location was an independent predictor of adverse LV remodeling (OR=1.061, p<0.001) and ejection-fraction at follow-up (Beta-coefficient=-0.255, p<0.001).

Coronary artery disease in patients aged 35 or less - A different beast?

Aim:To assess the extent and severity of coronary artery disease (CAD) in 200 consecutive patients aged 35 years or less undergoing diagnostic coronary angiography.Patients and Methods:Findings in these 200 patients (≤ 35 years of age) were analyzed to find the extent and severity of CAD. The mean age was 31.69 (±3.76) years. Majority were males (94%) and from the Arab ethnicity (70.5%).Result:Smoking (71%) and history of premature CAD (27%) were the most frequent risk factors (RF). History of previous ST elevation myocardial infarction (MI) was present in 68%. Anterior wall MI was the most frequent location (63.3%). The majority (54.3%) had moderate or large size MI. Ejection fraction (EF) less than 50% was noted in 30.3%. Left main or triple vessel CAD was seen in 15%. One- and two-vessel CAD was seen in 32.5% and 19% patients, respectively. Coronary angiogram was completely normal in 23.5%. The majority (54.5%) were treated conservatively and the rest (45.5%) needed percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG). The mean number of stents used was 1.3 ± 0.67 and the mean length of stents used was 20.3 ± 12.6 mm.Conclusion:The extent and severity of CAD was very significant in this subgroup of very young (≤35 years) Asian patients. Smoking was the main risk factor and half of the patients needed either PCI or CABG.