Impact of sleep-disordered breathing on myocardial salvage and infarct size in patients with acute myocardial infarction.

AIMS: Sleep-disordered breathing (SDB) may be a risk factor for expansion of infarct size early after acute myocardial infarction (MI) by exposing the heart to repetitive oxygen desaturations and increased cardiac afterload. The objective of this study was to assess the impact of SDB on myocardial salvage and infarct size within 3 months after acute MI. METHODS AND RESULTS: Patients with acute MI and percutaneous coronary intervention were enrolled in this prospective observational study. All patients underwent cardiovascular magnetic resonance (CMR) to define salvaged myocardium and infarct size within three to five days and at 3 months after acute MI. Patients were stratified according to apnoea-hypopnoea index (AHI) assessed by polysomnography at baseline into those with (AHI ≥ 15/h) and without (AHI < 15/h) SDB. Of the 56 patients included, 29 (52%) had SDB. The area at risk between both groups was similar (40 ± 12% vs. 40 ± 14%, P = 0.925). Patients with SDB had significantly less salvaged myocardium (myocardial salvage index 52% vs. 77%, P < 0.001), smaller reduction in infarct size (0.3% vs. 6.5%, P < 0.001) within 3 months after acute MI, a larger final infarct size (23% vs. 12%, P < 0.001), and a lower final left ventricular ejection fraction (48% vs. 54%, P = 0.023). In a multivariate analysis, including established risk factors for large MI, AHI was independently associated with less myocardial salvage and a larger infarct size 3 months after acute MI. CONCLUSIONS: Sleep-disordered breathing was associated with less myocardial salvage and a smaller reduction in infarct size. These findings suggest a contribution of SDB to impaired healing of MI.

Tumor marker carbohydrate antigen 125 predicts adverse outcome after transcatheter aortic valve implantation.

OBJECTIVES: This study sought to predict the value of tumor marker carbohydrate antigen 125 (CA125) before and after transcatheter aortic valve implantation (TAVI) for all-cause death and a composite endpoint of death, admission for heart failure, myocardial infarction, and stroke (major adverse cardiac events [MACE]). BACKGROUND: Risk stratification after TAVI remains challenging. The use of biomarkers in this setting represents an unmet need. METHODS: CA125 was measured in 228 patients before and after TAVI. The association with outcomes was assessed using parametric Cox regression and joint modeling for baseline and longitudinal analyses, respectively. CA125 was evaluated as logarithm transformation and dichotomized by its median value (M1 ≤15.7 U/ml vs. M2 >15.7 U/ml). RESULTS: At a median follow-up of 183 days (interquartile range: 63 to 365) and 144 days (interquartile range: 56 to 365), 50 patients (22%) died and 75 patients (33%) experienced MACE. A 3-fold increase in the rates for death and MACE was observed in patients above the median (M2 vs. M1) of CA125 (5.2 vs. 1.6 per 10 person-years and 8.3 vs. 3.3 per 10 person-years, respectively; p for both <0.001). In a multivariable analysis adjusted for logistic EuroSCORE, New York Heart Association functional class III/IV, and device success, baseline values of CA125 (M2 vs. M1) independently predicted death (hazard ratio [HR]: 2.18; 95% confidence interval [CI]: 1.11 to 4.26; p = 0.023) and MACE (HR: 1.77; 95% CI: 1.05 to 2.98; p = 0.031). In the longitudinal analysis, lnCA125 as a time-varying exposure, was highly associated with both endpoints: HR: 1.47; 95% CI: 1.01 to 2.14; p = 0.043 and HR: 2.26; 95% CI: 1.28 to 3.98; p = 0.005, for death and MACE, respectively. CONCLUSIONS: Serum levels of CA125 before and after TAVI independently predict death and MACE.

Prosthesis sizing for transcatheter aortic valve implantation--comparison of three dimensional transesophageal echocardiography with multislice computed tomography.

BACKGROUND: The complex anatomy of the aortic annulus warrants the use of three dimensional (3D) modalities for prosthesis sizing in transcatheter aortic valve implantation (TAVI). Multislice computed tomography (MSCT) has been used for this purpose, but its use may be restricted because of contrast administration. 3D transesophageal echocardiography (3D-TEE) lacks this limitation and data on comparison with MSCT is scarce. We compared 3D-TEE with MSCT for prosthesis sizing in TAVI. METHODS: Aortic annulus diameters in the sagittal and coronal plane and annulus areas in 3D-TEE and MSCT were compared in 57 patients undergoing TAVI. Final prosthesis size was left at the operator's discretion and the agreement with 3D-TEE and MSCT was calculated. RESULTS: Sagittal diameters on 3D-TEE and MSCT correlated well (r=.754, p<.0001) and means were comparable (22.3±2.1 vs. 22.5±2.3 mm; p=0.2; mean difference: -0.3 mm [-3.3-2.8]). On 3D-TEE, coronal diameter and annulus area were significantly smaller (p<.0001 for both) with moderate correlation (r=0.454 and r=0.592). Interobserver variability was comparable for both modalities. TAVI was successful in all patients with no severe post-procedural insufficiency. Final prosthesis size was best predicted by sagittal annulus diameters in 84% and 79% by 3D-TEE and MSCT, respectively. Agreement between both modalities was 77%. CONCLUSIONS: Annulus diameters and areas for pre-procedural TAVI assessment by 3D-TEE are significantly smaller than MSCT with exception of sagittal diameters. Using sagittal diameters, both modalities predicted well final prosthesis size and excellent procedural results were obtained. 3D-TEE can thus be a useful alternative in patients with contraindications to MSCT.

Cardiac workload in patients with sleep-disordered breathing early after acute myocardial infarction.

BACKGROUND: Sleep-disordered breathing (SDB) may promote an increase in cardiac workload early after acute myocardial infarction (AMI). We tested the hypothesis that in the early phase after AMI, SDB is associated with increased 24-h arterial BP, heart rate (HR), and, thus, cardiac workload. METHODS: In this prospective study, 55 consecutive patients with AMI and subsequent percutaneous coronary intervention (78% men; mean age, 54 ± 10 y; mean BMI, 28.3 ± 3.6 kg/m²; mean left ventricular ejection fraction [LVEF], 47% ± 8%) underwent polysomnography and 24-h ambulatory BP and heart rate monitoring within 5 days after MI. Cardiac workload was calculated as systolic BP multiplied by HR. The presence of SDB was defined as ≥ 10 apneas and hypopneas per hour of sleep. RESULTS: Fifty-five percent of the patients had SDB, of which 40% was predominantly central in nature. Patients with SDB had higher 24-h HR and systolic and diastolic BP compared with those without SDB (115 vs 108 mm Hg, P = .029; 71 vs 67 mm Hg, P = .034; 69 vs 64 beats/min, P = .050, respectively). Use of antihypertensive medication and ß-receptor blockers was similar in both groups. In a multivariate linear regression analysis, SDB was significantly associated with an increased 24-h cardiac workload (ß-coefficient, 0.364; 95% CI, 0.071-0.657; P = .016), independently of age, sex, BMI, LVEF, and antihypertensive medication. CONCLUSION: Patients with AMI and SDB have significantly increased 24-h BP, HR, and cardiac workload. Treatment of SDB may be a valuable nonpharmacologic approach to lower cardiac workload in these patients.

Emergency and prophylactic use of miniaturized veno-arterial extracorporeal membrane oxygenation in transcatheter aortic valve implantation.

OBJECTIVES: To report our center's experience using veno-arterial extracorporeal membrane oxygenation (vaECMO) in transcatheter aortic valve implantation (TAVI). BACKGROUND: In TAVI, short-term mortality closely relates to life threatening procedural complications. VaECMO can be used to stabilize the patient in emergency situations. However, for the prophylactic use of vaECMO in very high-risk patients undergoing TAVI there is no experience. METHODS: From January 2009 to August 2011, we performed 131 TAVI. Emergency vaECMO was required in 8 cases (7%): ventricular perforation (n = 3), hemodynamic instability/cardiogenic shock (n = 4), hemodynamic deterioration due to ventricular tachycardia (n = 1). Since August 2011, during 83 procedures, prophylactic vaECMO was systematically used in very high-risk patients (n = 9, 11%) and emergency ECMO in one case (1%) due to ventricular perforation. RESULTS: Median logistic EuroScore in prophylactic vaECMO patients was considerably higher as compared to the remaining TAVI population (30% vs. 15%, P = 0.0003) while in patients with emergency vaECMO it was comparable (18% vs. 15%, P = 0.08). Comparing prophylactic to emergency vaECMO, procedural success and 30-day mortality were 100% vs. 44% (P = 0.03) and 0% vs. 44% (P = 0.02), respectively. Major vascular complications and rate of life threatening bleeding did not differ between both groups (11% vs. 11%, P = 0.99 and 11% vs. 33%, P = 0.3) and were not vaECMO-related. CONCLUSIONS: Life-threatening complications during TAVI can be managed using emergency vaECMO but mortality remains high. The use of prophylactic vaECMO in very high-risk patients is safe and may be advocated in selected cases.

Cardiovascular magnetic resonance-derived intramyocardial hemorrhage after STEMI: Influence on long-term prognosis, adverse left ventricular remodeling and relationship with microvascular obstruction.

BACKGROUND: T2 weighted cardiovascular magnetic resonance (CMR) can detect intramyocardial hemorrhage (IMH) after ST-elevation myocardial infarction (STEMI). The long-term prognostic value of IMH beyond a comprehensive CMR assessment with late enhancement (LE) imaging including microvascular obstruction (MVO) is unclear. The value of CMR-derived IMH for predicting major adverse cardiac events (MACE) and adverse cardiac remodeling after STEMI and its relationship with MVO was analyzed. METHODS: CMR including LE and T2 sequences was performed in 304 patients 1 week after STEMI. Adverse remodeling was defined as dilated left ventricular end-systolic volume indexes (dLVESV) at 6 months CMR. RESULTS: During a median follow-up of 140 weeks, 47 MACE (10 cardiac deaths, 16 myocardial infarctions, 21 heart failure episodes) occurred. Predictors of MACE were ejection fraction (HR .95 95% CI [.93-.97], p=.001, per %) and IMH (HR 1.17 95% CI [1.03-1.33], p=.01, per segment). The extent of MVO and IMH significantly correlated (r=.951, p<.0001). dLVESV was present in 40% of patients. CMR predictors of dLVESV were: LVESV (OR 1.11 95% CI [1.07-1.15], p<.0001, per ml/m(2)), infarct size (OR 1.05 95% CI [1.01-1.09], p=.02, per %) and IMH (OR 1.54 95% CI [1.15-2.07], p=.004, per segment). Addition of T2 information did not improve the LE and cine CMR-model for predicting MACE (.744 95% CI [.659-.829] vs. .734 95% CI [.650-.818], p=.6) or dLVESV (.914 95% CI [.875-.952] vs. .913 95% CI [.875-.952], p=.9). CONCLUSIONS: IMH after STEMI predicts MACE and adverse remodeling. Nevertheless, with a strong interrelation with MVO, the addition of T2 imaging does not improve the predictive value of LE-CMR.

Predictors of cardiovascular magnetic resonance-derived microvascular obstruction on patient admission in STEMI.

BACKGROUND: Early stratification of patients according to the risk for developing microvascular obstruction (MVO) after ST-segment elevation myocardial infarction (STEMI) is desirable. We aimed to identify predictors of cardiovascular magnetic resonance (CMR)-derived MVO from clinical+ECG, laboratory and angiographic parameters available on admission. METHODS: Characteristics available on admission were documented in 97 STEMI patients referred for primary angioplasty. MVO was determined using contrast-enhanced CMR. RESULTS: MVO was present in 44 patients (45%). The C-statistic for predicting MVO was: clinical+ECG (.832), laboratory (.743), and angiographic parameters (.669). Adding laboratory to clinical+ECG information did not improve the C-statistic (.873 vs. .832, p=.2). Further addition of angiographic data (.904) improved the C-statistic of clinical+ECG (p=.04) but not of clinical+ECG and laboratory (p=.2). Independent predictors of MVO using clinical and ECG parameters were: Killip class >1 (OR 15.97 95%CI [1.37-186.76], p=.03), diabetes (OR 6.15 95%CI [1.49-25.39], p=.01), age <55years (OR 4.70 95%CI [1.56-14.17], p=.006), sum of ST-segment elevation >10mm (OR 4.5 95%CI [1.58-12.69], p=.005) and delayed presentation >3h (OR 3.80 95%CI [1.19-12.1], p=.02). A score was constructed assigning Killip class >1 2 points and the remaining indexes 1 point. The incidence of MVO increased with the score: 0 point: 8.7%; 1 point: 28.1%; 2 points: 71.4%; and 3+ points: 93% (p<.0001). CONCLUSIONS: MVO can be predicted using parameters already available on patient admission. We developed a clinical-ECG score allowing for early and reliable classification of STEMI patients according to the risk of MVO.

Natural course of sleep-disordered breathing after acute myocardial infarction.

The aim of this study was to test whether an improvement of left ventricular ejection fraction (EF) in the early phase after acute myocardial infarction is associated with a reduction of the severity of central and obstructive sleep apnoea. 40 consecutive patients with acute myocardial infarction underwent polysomnography and cardiovascular magnetic resonance imaging within 5 days and 12 weeks after the event to assess sleep apnoea and cardiac function. We stratified the sample in patients who improved their left ventricular EF within 12 weeks by ≥ 5% (improved EF group, ΔEF 9 ± 1%, n=16) and in those who did not (unchanged EF group, ΔEF -1 ± 1%, n=24). Prevalence of sleep apnoea (≥ 15 apnoea and hypopnoea events·h(-1)) within ≤ 5 days after myocardial infarction was 55%. Apnoea and hypopnoea events·h(-1) were significantly more reduced in the improved EF group compared with the unchanged EF group (-10 ± 3 versus 1 ± 3 events·h(-1); p=0.036). This reduction was based on a significant alleviation of obstructive events (-7 ± 2 versus 4 ± 3 events·h(-1); p=0.009), while the reduction of central events was similar between groups (p=0.906). An improvement of cardiac function early after myocardial infarction is associated with an alleviation of sleep apnoea. This finding suggests that re-evaluation of treatment indication for sleep apnoea is needed when a change in cardiac function occurs.

Impact of three-dimensional transesophageal echocardiography on prosthesis sizing for transcatheter aortic valve implantation.

OBJECTIVES: To compare aortic annulus diameters obtained by 3D transesophageal echocardiography (TEE) with 2D-TEE and the impact on prosthesis size selection in transcatheter aortic valve implantation (TAVI). BACKGROUND: In TAVI the aortic annulus diameter determines prosthesis size. The ideal modality for annulus assessment has not been defined yet. METHODS: Annulus diameters in 2D-TEE (long-axis view) and in 3D-TEE (long-axis view in multiple-plane-reconstruction) were compared in consecutive patients with aortic stenosis screened for TAVI. Prosthesis size was selected according to industry guidelines, integrating data from 3D-TEE, angiography and computed tomography. The percentage of cases in which 2D-TEE and 3D-TEE correctly predicted final prosthesis size was calculated. RESULTS: Forty-nine patients were studied (Age 80 ± 5, 39% male, logistic EuroScore 17 ± 11%). Annulus diameters from 2D- and 3D-TEE correlated (r = 0.808, P < 0.0001). Mean diameters were significantly larger on 3D- vs. 2D-TEE (23.4 ± 2.2 vs. 22.1 ± 2.6 mm, P < 0.001) with a mean difference of 1.2 mm (limits of agreement: -1.8 to 4.3). The interobserver variability of 2D- and 3D-TEE was 3.5 ± 5.6% and 0.9 ± 5.1%, respectively. Thirty-nine patients underwent TAVI (27 CoreValve™, 12 Edwards Sapien™). The procedure was successful in 37 (95%) patients. Postprocedural regurgitation was none or mild in 89% of the cases with no severe insufficiency. Final prosthesis size was correctly predicted by 2D-TEE in 67% while in 80% by 3D-TEE. Overall, 3D-TEE suggested a different prosthesis size in 26% of all cases compared to 2D-TEE. CONCLUSIONS: Aortic annulus measurement by 3D-TEE yields significantly larger diameters than 2D-TEE. This impacts prosthesis size selection in a considerable percentage of cases.

Function of remote non-infarcted myocardium after STEMI: analysis with cardiovascular magnetic resonance.

To evaluate remote myocardial function after ST-elevation myocardial infarction (STEMI) and the impact of infarct size (IS) using cardiovascular magnetic resonance (CMR). 161 patients and 15 controls underwent CMR at 1st week and 6th month after STEMI. Using the 17-segments model, segments were categorized into infarcted, adjacent and remote myocardium. Relative systolic wall thickening (SWT, %) was assessed using the centerline method. IS (% of left ventricular mass) was determined in late enhancement imaging. Overall, in remote myocardium, SWT was comparable (83 ± 32) to controls (77 ± 25, P = .5) and did not increase significantly (P = .2) at the 6th month (88 ± 35, P = .3 vs. control). When IS was categorized into tertiles (<13.6%, (n = 49), 13.7-28.2%, (n = 60), >28.2%, (n = 52)), SWT in the remote area at the 1st week was not different from controls, regardless of infarct size (p between .2 and .8 for all tertiles). At 6 months, SWT was larger compared to controls only in small infarctions (98 ± 34 vs. 77 ± 25, P = .03). In medium and large infarctions there was no difference in SWT of the remote area compared to controls (87 ± 33 and 79 ± 34, P = .3 and P = .09) and there was no significant increase at 6 months (P between .2 and .9). In remote myocardium there was no difference in contractility compared to controls after STEMI. After 6 month a slight hypercontractility can only be observed in small infarctions. In medium and large infarctions no difference of SWT in remote myocardium compared to controls can be observed.

A simple method of vascular access to perform emergency coronary angiography in patients with veno-arterial extracorporeal membrane oxygenation.

PURPOSE: Veno-arterial extracorporeal membrane oxygenation (V-A ECMO) is progressively used in severe cardiogenic shock or in-hospital resuscitation to stabilize patients and to bridge to further therapeutic interventions. However, vascular access for coronary catheterization can be difficult under these conditions. It would thus be desirable to use arterial lines that are already inserted. Here, we describe a novel technique to perform coronary angiography and angioplasty in patients with V-A ECMO. METHODS: The technique is described in five patients in whom V-A ECMO was established because of prolonged cardiopulmonary resuscitation and who underwent coronary catheterization after stabilization. At the arterial cannula of the ECMO, a Y connector was inserted. At its free end, a hemostatic valve was placed, over which the coronary catheters were inserted. RESULTS: In one case, diagnostic coronary angiography revealed no significant coronary stenosis. In four other cases, successful coronary angioplasty with and without stent implantation was performed. CONCLUSION: Cardiac catheterization using a Y-shaped adapter introduced into the arterial ECMO cannula is feasible. In a resuscitation setting, a new puncture of the femoral artery always carries the risk of complications, wherefore this new technology can be regarded as fast alternative.

Eplerenone prevents salt-induced vascular stiffness in Zucker diabetic fatty rats: a preliminary report.

BACKGROUND: Aldosterone levels are elevated in a rat model of type 2 diabetes mellitus, the Zucker Diabetic fatty rat (ZDF). Moreover blood pressure in ZDF rats is salt-sensitive. The aim of this study was to examine the effect of the aldosterone antagonist eplerenone on structural and mechanical properties of resistance arteries of ZDF-rats on normal and high-salt diet. METHODS: After the development of diabetes, ZDF animals were fed either a normal salt diet (0.28%) or a high-salt diet (5.5%) starting at an age of 15 weeks. ZDF rats on high-salt diet were randomly assigned to eplerenone (100 mg/kg per day, in food) (ZDF+S+E), hydralazine (25 mg/kg per day) (ZDF+S+H), or no treatment (ZDF+S). Rats on normal salt-diet were assigned to eplerenone (ZDF+E) or no treatment (ZDF). Normoglycemic Zucker lean rats were also divided into two groups receiving normal (ZL) or high-salt diet (ZL+S) serving as controls. Systolic blood pressure was measured by tail cuff method. The experiment was terminated at an age of 25 weeks. Mesenteric resistance arteries were studied on a pressurized myograph. Specifically, vascular hypertrophy (media-to-lumen ratio) and vascular stiffness (strain and stress) were analyzed. After pressurized fixation histological analysis of collagen and elastin content was performed. RESULTS: Blood pressure was significantly higher in salt-loaded ZDF compared to ZDF. Eplerenone and hydralazine prevented this rise similarily, however, significance niveau was missed. Media-to-lumen ratio of mesenteric resistance arteries was significantly increased in ZDF+S when compared to ZDF and ZL. Both, eplerenone and hydralazine prevented salt-induced vascular hypertrophy. The strain curve of arteries of salt-loaded ZDF rats was significantly lower when compared to ZL and when compared to ZDF+S+E, but was not different compared to ZDF+S+H. Eplerenone, but not hydralazine shifted the strain-stress curve to the right indicating a vascular wall composition with less resistant components. This indicates increased vascular stiffness in salt-loaded ZDF rats, which could be prevented by eplerenone but not by hydralazine. Collagen content was increased in ZL and ZDF rats on high-salt diet. Eplerenone and hydralazine prevented the increase of collagen content. There was no difference in elastin content. CONCLUSION: Eplerenone and hydralazine prevented increased media-to-lumen ratio in salt-loaded ZDF-rats, indicating a regression of vascular hypertrophy, which is likely mediated by the blood pressure lowering-effect. Eplerenone has additionally the potential to prevent increased vascular stiffness in salt-loaded ZDF-rats. This suggests an effect of the specific aldosterone antagonist on adverse vascular wall remodelling.

Prognostic impact of sleep disordered breathing and its treatment in heart failure: an observational study.

AIMS: Sleep disordered breathing (SDB) may contribute to disease progression in patients with chronic heart failure (CHF). The objective of this observational study was to evaluate whether SDB is a risk factor for mortality in CHF patients and whether this risk can be attenuated by treatment with positive airway pressure (PAP). METHODS AND RESULTS: We studied 296 CHF patients (median left ventricular ejection fraction 33%) who underwent in-lab polysomnography between January 2002 and December 2009. We compared (i) mortality between patients with severe SDB [apnoea-hypopnoea index (AHI) ≥ 22.5 h(-1)] vs. those without severe SDB (AHI < 22.5 h(-1)) and (ii) evaluated the impact of PAP treatment on mortality in those with severe SDB. After accounting for significant confounding factors (age, NYHA class, cause of CHF, diabetes, and PAP treatment), patients with severe SDB (n= 176) had a 2.0-fold increased hazard ratio for death compared with those without severe SDB [95% confidence interval (CI) 1.1-3.5, P= 0.023]. In an adjusted on-treatment analysis of the group with severe SDB, mortality was significantly less in patients using PAP (18%) compared with those with untreated SDB (52%; hazard ratio 0.4, 95% CI 0.2-0.6, P= 0.001). Mortality in the PAP-treated group was lower compared with the untreated group at any time-point of the follow-up period. CONCLUSION: The presence of severe SDB in CHF patients constitutes a significantly increased risk for death, independent of established risk factors. In CHF patients with SDB, use of PAP therapy was associated with a decreased mortality rate at any time point of the follow-up, suggesting that PAP can be safely used in such patients.

White blood cell subtypes after STEMI: temporal evolution, association with cardiovascular magnetic resonance--derived infarct size and impact on outcome.

The evolution of white blood cells after ST elevation myocardial infarction (STEMI) and their association with infarct size and major adverse cardiac events (MACE) remains unclear. Two hundred eleven patients underwent CMR after STEMI. Infarct mass (grams) was determined. Neutrophil, lymphocyte, and monocyte counts (×1,000 cells/ml) were measured upon arrival and at 12, 24, 48, 72, and 96 h. Patients with large infarctions (3rd tertile ≥ 28.5 g vs. 1st and 2nd tertiles < 28.5 g) showed a larger neutrophil count at 12 h (14.8 ± 4.8 vs. 11.4 ± 3.3, p < 0.0001) and an increased monocyte count (maximum at 24 h (0.65[0.50-0.91] vs. 0.55[0.42-0.71], p = 0.004)) but no difference in lymphocyte count. Neutrophil count at 12 h independently predicted large infarctions (OR 1.14, 95%CI [1.04-1.26], p = 0.008). During follow-up (median 504 days), 25 MACE occurred. Neutrophil count at 96 h independently predicted MACE (HR 1.2, 95%CI [1.1-1.4], p = 0.003). Large infarctions show a marked neutrophil peak and an increasing monocyte count. Neutrophil count independently predicts large infarctions and MACE.

La suma de la elevación del segmento ST predice mejor la obstrucción microvascular en pacientes tratados con éxito con una intervención coronaria percutánea primaria. Un estudio de resonancia magnética cardiovascular / The sum of ST-segment elevation is the best predictor of microvascular obstruction in patients treated successfully by primary percutaneous coronary intervention. Cardiovascular magnetic resonance study

Introducción y objetivos. La utilidad de la resolución del segmento ST (RST) para la predicción de la reperfusión epicárdica está bien establecida. La asociación de los cambios del segmento ST con la obstrucción microvascular (OMV) observada en la resonancia magnética cardiovascular (RMC) tras una intervención coronaria percutánea primaria (ICPp) en el infarto de miocardio con elevación del ST (IMEST) no se ha aclarado todavía. Métodos. Estudiamos a 85 pacientes consecutivos ingresados por un primer IMEST y tratados con una ICPp que tenían una arteria relacionada con el infarto permeable. Se registró un ECG al ingreso, tras 90 min y tras 6, 24, 48 y 96 h de la ICPp. Se calculó la RST y la suma de la elevación del ST (sumEST) en todas las derivaciones. Resultados. La RMC reveló una OMV en 37 pacientes. En los infartos con OMV, el valor de la sumEST antes y después de la revascularización fue mayor que en los infartos sin OMV (p <= 0,001 en todos los casos). En cambio, no hubo diferencias significativas en la cantidad de RST entre los infartos con y sin OMV a los 90 min de la revascularización (p = 0,1), sino sólo a partir de las 6 h (p < 0,05 en todos los casos). El área bajo la curva de características operativas del receptor para la detección de la OMV fue mayor para la sumEST que para la RST (p < 0,05 en todas las determinaciones). En el análisis multivariable, ajustado respecto a las características clínicas, angiográficas y electrocardiográficas, una sumEST > 3 mm a los 90 min de la ICPp, pero no una RST >= 70%, predijo de manera independiente la OMV observada en la RMC (odds ratio = 3,1; intervalo de confianza del 95%, 1,2-8,4; p = 0,02). Conclusiones. La OMV se asoció a un valor significativamente superior de la sumEST en todos los momentos de valoración tras la revascularización. La diferencia en la cantidad de RST entre los infartos con OMV y sin OMV sólo fue significativa a partir de las 6 h tras la revascularización. La OMV se predijo mejor con una sumEST > 3 mm a los 90 min de la ICPp (AU)

Introduction and objectives. The usefulness of STsegment elevation resolution (STR) for predicting epicardial reperfusion is well established. However, it is still not clear how ST-segment changes are related to microvascular obstruction (MVO) observed by cardiovascular magnetic resonance (CMR) after primary percutaneous coronary intervention (pPCI) for ST-segment elevation myocardial infarction (STEMI). Methods. The study involved 85 consecutive patients admitted for a first STEMI and treated by pPCI who had a patent infarct-related artery. An ECG was recorded on admission and 90 min and 6, 24, 48 and 96 h after pPCI. Thereafter, STR and the sum of ST-segment elevation (sumSTE) in all leads were determined. Results. Overall, CMR revealed MVO in 37 patients. In infarcts with MVO, sumSTE was greater both before and after revascularization than in infarcts without MVO (P<=.001 at all times). In contrast, there was no significant difference in the magnitude of STR between infarcts with and without MVO 90 min after revascularization (P=.1), though there was after 6 h (P<.05 at all times). The area under the receiver operating characteristic curve for detecting MVO was greater for sumSTE than STR (P<.05 for all measurements). On multivariate analysis, after adjusting for clinical, angiographic and ECG characteristics, a sumSTE >3 mm 90 min after pPCI was an independent predictor of MVO on CMR, while an STR >=70% was not (odds ratio=3.1; 95% confidence interval, 1.2-8.4; P=.02). Conclusions. MVO was associated with a significantly increased sumSTE at all times after revascularization. The difference in the magnitude of STR between infarcts with and without MVO was significant only >6 h after revascularization. The best predictor of MVO was a sumSTE >3 mm 90 min after pPCI. Key words: Cardiovascular magnetic resonance. Microvascular obstruction. ST-segment resolution. Sum of ST-segment elevation. ST-segment elevation myocardial infarction (AU)

The sum of ST-segment elevation is the best predictor of microvascular obstruction in patients treated successfully by primary percutaneous coronary intervention. Cardiovascular magnetic resonance study.

INTRODUCTION AND OBJECTIVES: The usefulness of ST-segment elevation resolution (STR) for predicting epicardial reperfusion is well established. However, it is still not clear how ST-segment changes are related to microvascular obstruction (MVO) observed by cardiovascular magnetic resonance (CMR) after primary percutaneous coronary intervention (pPCI) for ST-segment elevation myocardial infarction (STEMI). METHODS: The study involved 85 consecutive patients admitted for a first STEMI and treated by pPCI who had a patent infarct-related artery. An ECG was recorded on admission and 90 min and 6, 24, 48 and 96 h after pPCI. Thereafter, STR and the sum of ST-segment elevation (sumSTE) in all leads were determined. RESULTS: Overall, CMR revealed MVO in 37 patients. In infarcts with MVO, sumSTE was greater both before and after revascularization than in infarcts without MVO (P≤.001 at all times). In contrast, there was no significant difference in the magnitude of STR between infarcts with and without MVO 90 min after revascularization (P=.1), though there was after 6 h (P< .05 at all times). The area under the receiver operating characteristic curve for detecting MVO was greater for sumSTE than STR (P< .05 for all measurements). On multivariate analysis, after adjusting for clinical, angiographic and ECG characteristics, a sumSTE >3 mm 90 min after pPCI was an independent predictor of MVO on CMR, while an STR ≥70% was not (odds ratio=3.1; 95% confidence interval, 1.2-8.4; P=.02). CONCLUSIONS: MVO was associated with a significantly increased sumSTE at all times after revascularization. The difference in the magnitude of STR between infarcts with and without MVO was significant only >6 h after revascularization. The best predictor of MVO was a sumSTE >3 mm 90 min after pPCI.

Association of early repolarization pattern on ECG with risk of cardiac and all-cause mortality: a population-based prospective cohort study (MONICA/KORA).

BACKGROUND: Early repolarization pattern (ERP) on electrocardiogram was associated with idiopathic ventricular fibrillation and sudden cardiac arrest in a case-control study and with cardiovascular mortality in a Finnish community-based sample. We sought to determine ERP prevalence and its association with cardiac and all-cause mortality in a large, prospective, population-based case-cohort study (Monitoring of Cardiovascular Diseases and Conditions [MONICA]/KORA [Cooperative Health Research in the Region of Augsburg]) comprised of individuals of Central-European descent. METHODS AND FINDINGS: Electrocardiograms of 1,945 participants aged 35-74 y, representing a source population of 6,213 individuals, were analyzed applying a case-cohort design. Mean follow-up was 18.9 y. Cause of death was ascertained by the 9th revision of the International Classification of Disease (ICD-9) codes as documented in death certificates. ERP-attributable effects on mortality were determined by a weighted Cox proportional hazard model adjusted for covariables. Prevalence of ERP was 13.1% in our study. ERP was associated with cardiac and all-cause mortality, most pronounced in those of younger age and male sex; a clear ERP-age interaction was detected (p = 0.005). Age-stratified analyses showed hazard ratios (HRs) for cardiac mortality of 1.96 (95% confidence interval [CI] 1.05-3.68, p = 0.035) for both sexes and 2.65 (95% CI 1.21-5.83, p = 0.015) for men between 35-54 y. An inferior localization of ERP further increased ERP-attributable cardiac mortality to HRs of 3.15 (95% CI 1.58-6.28, p = 0.001) for both sexes and to 4.27 (95% CI 1.90-9.61, p<0.001) for men between 35-54 y. HRs for all-cause mortality were weaker but reached significance. CONCLUSIONS: We found a high prevalence of ERP in our population-based cohort of middle-aged individuals. ERP was associated with about a 2- to 4-fold increased risk of cardiac mortality in individuals between 35 and 54 y. An inferior localization of ERP was associated with a particularly increased risk. Please see later in the article for the Editors' Summary.

Hyperaldosteronism and altered expression of an SGK1-dependent sodium transporter in ZDF rats leads to salt dependence of blood pressure.

This study was designed to test whether altered aldosterone-related sodium handling leads to salt-sensitive blood pressure in diabetes and thus may exaggerate end-organ damage. Zucker diabetic fatty (ZDF) rats, a model of type 2 diabetes, and Zucker lean (ZL) rats, as euglycemic controls, were divided into groups receiving normal (0.28%) (ZDF+N, ZL+N) and high-salt (5.5%) diets (ZDF+S, ZL+S) for 10 weeks. Renal mRNA expression of serum- and glucocorticoid-inducible kinase 1 (SGK1) and sodium transporters (for example, the epithelial sodium channel-α, ENaCα) were measured by quantitative reverse transcriptase-PCR. Vascular hypertrophy (media-to-lumen ratio, M/L) in mesenteric resistance arteries was assessed using a pressurized myograph. Systolic blood pressure (SBP) was significantly higher in ZDF+S vs. ZDF+N (146 ± 2 vs. 133 ± 3 mm Hg; P<0.05), whereas there was no difference between ZL+S and ZL+N (151 ± 3 vs. 147 ± 3 mm Hg). Plasma sodium concentration was higher in ZDF+S vs. ZDF+N, whereas there was no difference between ZL+S and ZL+N. Plasma aldosterone concentration (PAC) was higher in ZDF+N as compared with ZL+N (191 ± 23 vs. 95 ± 35 pg ml(-1); P<0.05). PAC decreased to zero in ZL+S, which was not the case in ZDF+S (0 ± 0 vs. 37 ± 2 pg ml(-1)). Salt loading decreased the mRNA expression of SGK1 in euglycemic controls (ZL+S 0.58 ± 0.2 vs. ZL+N 1.05 ± 0.05; P=0.05), whereas it significantly increased SGK1 expression in diabetic rats (ZDF+S 1.75 ± 0.15 vs. ZDF+N 0.92 ± 0.07; P<0.01). ENaCα mRNA expression paralleled these changes. The M/L of mesenteric resistance arteries was not different between ZDF+N and ZL+N. High salt significantly increased the M/L in ZDF+S vs. ZDF+N, but not in ZL+S vs. ZL+N. Systolic blood pressure in this model of type 2 diabetes mellitus is salt sensitive, leading to marked vascular remodeling. The underlying pathophysiological mechanism may be inappropriately high levels of aldosterone and up-regulation of SGK1-dependent renal sodium transport by ENaCα, leading to net increased sodium retention.

Variable phenotypes of bicuspid aortic valve disease: classification by cardiovascular magnetic resonance.

BACKGROUND: Recently, cardiovascular magnetic resonance (CMR) has been shown to allow accurate visualisation and quantification of aortic valve disease. Although bicuspid aortic valve (BAV) disease is relatively rare in the general population, the frequency is high in patients requiring valve surgery. The aim of the current study was to characterise the different phenotypes of BAV disease by CMR. METHODS: CMR studies were performed on a 1.5 T scanner in 105 patients with BAV. RESULTS: The pattern of BAV phenotypes was as follows: a raphe was identified in 90 patients (86%). Among patients with raphe, 76 patients had fusion between the right and left cusps (RL) and 14 patients had fusion between the right and the non-coronary cusps (RN). There were no significant differences in the aortic dimensions in the different BAV phenotypes. CONCLUSION: CMR allows excellent characterisation of valve phenotype in patients with BAV. The present data demonstrate that a raphe is present in the vast majority of cases and RL fusion is the predominant phenotype of BAV. No significant differences in the aortic dimensions were observed.

Dynamic changes in N-terminal pro-brain natriuretic peptide in acute coronary syndromes treated with percutaneous coronary intervention: a marker of ischemic burden, reperfusion and outcome.

BACKGROUND: Whereas N-terminal pro-brain natriuretic peptide (NT-proBNP) is approved for risk stratification of patients with acute coronary syndromes (ACS), short-term temporal changes in NT-proBNP concentrations and the optimal time points for sampling are not clear. The purpose of this study was to better define the short-term changes in NT-proBNP in relation to clinical presentation, reperfusion and prognostic value in patients with ACS, as well as to identify the optimum time points for sampling. METHODS: We studied daily plasma concentrations of NT-proBNP in 133 unselected patients with myocardial infarction (n=65), stable coronary artery disease (CAD, n=46) and no CAD (n=22) who underwent coronary angiography. RESULTS: Patients with non-ST-elevation myocardial infarction (NSTEMI) presented with markedly higher NT-proBNP than patients with ST-elevation myocardial infarction (STEMI) [1305 (741-3208) ng/L vs. 170 (70-424) ng/L, p<0.001]. Also, time to presentation from onset of pain was much longer in NSTEMI as compared to STEMI (>48 h vs. <6 h, p<0.001). Patients with NSTEMI also presented with higher NT-proBNP as compared with CAD [224 (98-732) ng/L] and no CAD [47 (26-102) ng/L; p<0.001, NSTEMI vs. both]. Following successful percutaneous coronary intervention [thrombolysis in myocardial infarction (TIMI) 3-flow established], NT-proBNP increased markedly within 24 h in patients with STEMI [718 (379-1338) ng/L, p<0.01 vs. 0 h], whereas no change in NT-proBNP was noted in patients with NSTEMI [1190 (1010-2024) ng/L, p=0.88 vs. 0 h]. In both STEMI and NSTEMI, NT-proBNP decreased significantly 96 h after successful reperfusion [STEMI -52%, 372 (189-610) ng/L, p<0.05; NSTEMI -52%, 613 (365-724) ng/L, p<0.05]. Unsuccessful reperfusion (TIMI<3) was associated with unchanged or increased NT-proBNP. NT-proBNP at 96 h and peak NT-proBNP further displayed a strong correlation with cardiac troponin T (r=0.64 and r=0.54, p<0.001), a marker of infarct size, and NT-proBNP at 96 h was a strong predictor of long-term prognosis (hazard ratio 7.29, p=0.025). CONCLUSIONS: In patients with NSTEMI, NT-proBNP may be increased as high as concentrations usually associated with acute congestive heart failure despite the absence of clinical signs. In contrast, patients with STEMI and short time to presentation may present with completely normal NT-proBNP, but dramatic short-term increases following reperfusion. NT-proBNP reflects ischemic burden, reperfusion success and prognosis, and the current data support repetitive sampling in patients with ACS.