Cardiac Magnetic Resonance Shows Improved Outcomes in Patients with an ST-Segment Elevation Myocardial Infarction and a High Thrombus Burden Treated with Adjuvant Aspiration Thrombectomy.

There is a discrepancy between epicardial vessel patency and microcirculation perfusion in a third of patients treated with percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI). Optimization with aspiration thrombectomy (AT) may reduce distal embolization and microvascular obstruction. The effect of AT in the treatment of STEMI is debatable. The purpose of this study was to use cardiac magnetic resonance (CMR) to determine whether AT influences microvascular obstruction (MVO), infarct size and left ventricular (LV) remodelling in STEMI patients. Sixty STEMI patients with a thrombus-occluded coronary artery were randomized in a 2:1 fashion to receive PCI proceeded by AT (AT + PCI group), or PCI only. MVO, myocardial infarct size and LV remodelling were assessed by CMR during the index hospitalization and 6 months thereafter. The majority of patients had a large thrombus burden (TIMI thrombus grade 5 in over 70% of patients). PCI and AT were effective in all cases. There were no periprocedural strokes. CMR showed that the addition of AT to standard PCI was associated with lesser MVO when indexed to the infarct size and larger infarct size reduction. There were less patients with left ventricle remodelling in the AT + PCI vs. the PCI only group. To conclude, in STEMI patients with a high thrombus burden, AT added to PCI is effective in reducing infarct size, MVO and LV remodelling.

Infarct size and long-term left ventricular remodelling in acute myocardial infarction patients subjected to transcoronary delivery of progenitor cells.

Introduction: Infarct size (IS) is a fundamental determinant of left-ventricular (LV) remodelling (end-systolic and end-diastolic volume change, ΔESV, ΔEDV) and adverse clinical outcomes after myocardial infarction (MI). Our prior work found that myocardial uptake of transcoronary-delivered progenitor cells is governed by IS. Aim: To evaluate the relationship between IS, stem cell uptake, and the magnitude of LV remodelling in patients receiving transcoronary administration of progenitor cells shortly after MI. Material and methods: Thirty-one subjects (age 36-69 years) with primary percutaneous coronary intervention (pPCI)-treated anterior ST-elevation MI (peak CK-MB 584 [181-962] U/l, median [range]) and sustained left ventricle ejection fraction (LVEF) ≤ 45% were studied. On day 10 (median) 4.3 × 106 (median) autologous CD34+ cells (50% labelled with 99mTc-extametazime) were administered via the infarct-related artery (left anterior descending). ΔESV, ΔEDV, and mid circumferential myocardial strain (mCS) were evaluated at 24 months. Results: Infarct mass (cMRI) was 57 [11-112] g. Cell label myocardial uptake (whole-body γ-scans) was proportional to IS (r = 0.62), with a median 2.9% uptake in IS 1st tercile (≤ 45 g), 5.2% in 2nd (46-76 g), and 6.7% in 3rd (> 76 g) (p = 0.0006). Cell uptake in proportion to IS attenuated the IS-ΔESV (p = 0.41) and IS-ΔEDV (p = 0.09) relationship. At 24 months, mCS improved in IS 2nd tercile (p = 0.028) while it showed no significant change in smaller (p = 0.87) or larger infarcts (p = 0.58). Conclusions: This largest human study with labelled CD34+ cell transplantation shortly after MI suggests that cell uptake (proportional to IS) may attenuate the effect of IS on LV adverse remodelling. To boost this effect, further strategies should involve cell types and delivery techniques to maximize myocardial uptake.

Effect of ventricular function and volumes on exercise capacity in adults with repaired Tetralogy of Fallot.

OBJECTIVES: Investigate the effects of left and right ventricular function and severity of pulmonary valve regurgitation, quantified by cardiac magnetic resonance (CMR), on exercise tolerance in adult patients who underwent ToF repair at a young age. METHODS: This is a retrospective cohort study of 52 patients after ToF surgery and 33 age- and sex-matched healthy volunteers. CMR and cardiopulmonary exercise testing (CPET) were performed on all patients; CPET was performed on control subjects. RESULTS: The main finding of CPET was a severe decrease in oxygen uptake at peak exercise VO2peak in TOF patients. The patients were characterized also by lower pulse O2peak and heart rate at peak exercise. Ejection fraction of the right and left ventricles was correlated (r=0,32; p=0,03). Left ventricle ejection fraction was negatively correlated with right ventricular volumes (r=-0,34; p=0,01) and right ventricular mass (r=-046; p<0,00). Right ventricular mass was positively correlated with left ventricular variables (left ventricle end diastolic volume, r=0,43; p=0,002; left ventricle end systolic volume, r=0,54; p<0,00) as was VO2peak: LVEDV (r=0,38; p=0,01); LVESV (r=0,33; p=0,03) and LV mass (r=0,42; p=0,006). CONCLUSION: Exercise intolerance in adults with repaired ToF is markedly depressed. The decreased exercise capacity is correlated with impaired RV function and may be associated also with LV dysfunction, which suggests right-to-left ventricular interaction.

Right atrium enlargement predicts clinically significant supraventricular arrhythmia in patients with pulmonary arterial hypertension.

BACKGROUND: Right atrial (RA) enlargement is a common finding in patients with pulmonary arterial hypertension (PAH) and an important predictor of mortality, however its relation to the risk of atrial arrhythmias has not been assessed. OBJECTIVES: To assess whether RA enlargement is associated with supraventricular arrhythmias (SVA) and whether it predicts new clinically significant SVA (csSVA). METHODS: Patients with PAH were recruited between January 2010 and December 2014 and followed until January 2017. csSVA was diagnosed if it resulted in hospitalization. To assess predictors of new csSVA, only patients without a history of SVA at baseline were analyzed. RESULTS: Among 97 patients, any SVA was observed in 45 (46.4%) and included permanent atrial fibrillation(AF, n = 8), paroxysmal AF (n = 10), permanent atrial flutter (AFl, n = 1), paroxysmal AFl (n = 2) or other types of supraventricular tachycardia (n = 24). Patients with SVA as compared to patients without SVA were characterized by older age, lower distance in a 6-minute test, higher NT-proBNP, higher RA area index (RAai), left atrial area index, mean right atrial pressure (mRAP) and were more commonly treated with ß-blocker. Eighty five patients who were in sinus rhythm at baseline assessment and had no history of significant SVA were observed for 37 ± 19.9 months. During that time csSVA occurred in 15.3%. In univariate models, the occurrence of csSVA were predicted by age, right ventricular ejection fraction, right ventricular end diastolic index, RAai and mRAP, but in multivariate model only RAai remained significant predictor for csSVA (HR of 1.23, 95%CI: 1.11-1.36, p < 0.001). The optimal threshold for RA enlargement as discriminator of csSVA was 21.7 cm2/m2. CONCLUSIONS: In PAH patients RA enlargement is associated with increased prevalence of SVA. RAai is an independent predictor of hospitalization due to csSVA.

Fulminant adrenergic myocarditis complicated by pulmonary edema, cardiogenic shock and cardiac arrest.

Adrenergic myocarditis is an uncommon presentation of pheochromocytoma and extremely rare cause of de novo acute heart failure (AHF). We present a case of a 31-year-old Caucasian woman with a history of hypertension and recurrent occipital headaches who was admitted to the emergency department due to severe de novo AHF presenting as pulmonary edema and cardiogenic shock. During the hospital admission the patient experienced asystolic cardiac arrest and was successfully resuscitated, intubated, and mechanically ventilated. Bedside transthoracic echocardiography revealed severe diffuse left ventricular hypokinesis with ejection fraction (LVEF) of 10%. Coronary angiography disclosed normal epicardial coronary arteries. The diagnosis of fulminant myocarditis was based on clinical, laboratory and imaging findings including cardiac magnetic resonance imaging (cMRI) Lake Louise criteria. STIR-cMRI sequences revealed myocardial edema in the lateral, inferior and posterior walls of the left ventricle, whereas T1-weighted early contrast-enhanced sequences showed myocardial hyperemia and capillary leak. An ultrasound and computed tomographic scan of the abdomen disclosed a solid, heterogeneous mass (3.6×3.2×2.8-cm) in the right suprarenal area. Urinary and plasma catecholamines and metanephrines were markedly elevated. A pheochromocytoma was suspected and laparoscopic resection of the tumor was performed after pharmacological preparation with phenoxybenzamine. The histopathological findings were consistent with pheochromocytoma. Follow-up cMRI showed complete reversal of myocardial edema and hyperemia. At 12-month follow-up, the patient has remained asymptomatic and normotensive with no recurrence of cardiovascular symptoms.

Right Ventricular Epicardial Vascularisation in Patients With Pulmonary Arterial Hypertension.

BACKGROUND: Pulmonary arterial hypertension (PAH) leads to a haemodynamic overload and ischaemia of the right ventricle (RV), which are important triggers of an arterial growth. Thus, we aimed to assess whether patients with PAH have altered epicardial vasculature of the RV, and how it corresponds to RV haemodynamic stress. METHODS: We enrolled consecutive patients with PAH diagnosed in a single pulmonary hypertension centre, who underwent coronary angiography. The control group consisted of patients with normal coronary arteries. Artery branches from segments I-III of the right coronary artery (RCAB) and branches of the left coronary artery (LCAB) were assessed. The sum of the diameters of RCABs (RCAB_sum) was used as a marker of RV epicardial vascularisation. Linear regression models were used to investigate associations between the RCAB_sum and markers of RV dysfunction. RESULTS: We recruited 37 PAH patients (idiopathic, n=25; associated with connective tissue disease, n=12) and 37 control subjects of similar age (56±18 vs. 56±13 years, p=0.99) and sex (73% vs. 73% of women, p=0.99). Pulmonary arterial hypertension patients as compared with control subjects had more RCABs (7 [6-8] vs. 6 [5-7], p<0.001) and increased RCAB_sum (9.4 [8.2-10.5] vs. 7.3 [6.6-7.40] mm; p<0.001) although comparable LCAB count (4 [4-5] vs. 4 [4-5]; p=0.50). In a stepwise multivariable linear regression model, RA area (ß=0.152 [0.062-0.242]; p=0.002) and diastolic wall stress (ß=0.025 [0.005-0.045]; p=0.02) were significant predictors of RCAB_sum (model R2=0.65; p<0.0001). CONCLUSIONS: Right ventricular epicardial vasculature is more extensive in PAH patients as compared with control subjects, and it is in linear relation to potential markers of RV diastolic dysfunction.

Mechanism and prognostic role of qR in V1 in patients with pulmonary arterial hypertension.

BACKGROUND: The presence of qR pattern in lead V1 of the 12-lead surface ECG has been proposed as a risk marker of death in patients with pulmonary arterial hypertension (PAH). We aimed to validate these findings in the modern era of PAH treatment and additionally to assess the relation of qR in V1 to PAH severity. We also investigated the possible mechanisms underlying this ECG sign. METHODS: Consecutive patients with PAH excluding patients with congenital heart defect were recruited between February 2008 and January 2016. A 12-lead standard ECG was acquired and analyzed for the presence of qR in V1 and other potential prognostic patterns. Cardiac magnetic resonance and echocardiography were used for structural (masses and volumes) and functional (ejection fraction, eccentricity index) characterization of left (LV) and right (RV) ventricles. Standard markers of PAH severity were also assessed. RESULTS: We enrolled 66 patients (19 males), aged 50.0±15.7years with idiopathic PAH (n=52) and PAH associated with connective tissue disease (n=14). qR in V1 was present in 26(39.4%) patients and was associated with worse functional capacity, hemodynamics and RV function. The main structural determinants of qR in V1 were RV to LV volume ratio (OR: 3.99; 95% CI: 1.47-10.8, p=0.007) and diastolic eccentricity index (OR: 15.0; 95% CI: 1.29-175.5, p=0.03). During observation time of 30.5±19.4months, 20 (30.3%) patient died, 13 (50%) patients with qR and 7 (17.5%) patients without qR pattern. Electrocardiographic determinants of survival were qR (HR: 3.06, 95% CI: 1.21-7.4; p=0.02) and QRS duration (HR: 1.02, 95% CI: 1.01-1.04; p=0.01). CONCLUSIONS: Presence of qR in V1 reflects RV dilation and diastolic interventricular septum flattening. It is a sign of advanced PAH and predicts the risk of death in this population.

Long-term follow-up after Holmium:YAG laser revascularization combined with autologous bone marrow derived stem cells implantation.

Background: Coronary artery disease is a major cause of death worldwide. Despite different standard revascularization options, significant number of patients remains not suitable for any treatment. The aim of the study was to evaluate long-term outcome of patients with diffuse coronary artery disease, treated with autologous stem cells injections combined with transmyocardial laser revascularization. Material and Methods: 9 patients underwent Holmium:YAG laser revascularization and autologous bone marrow derived stem cells implantation between 2007 and 2009 in the Department of Cardiovascular Surgery and Transplantology, John Paul II Hospital, Kraków and were subsequently followed up in 2015. Results: The mean follow-up period was 73 months. The mean CCS class significantly improved (1.4±0.5 vs 3.3±1.0; p<0.001) and cardiac related hospitalizations significantly decreased (1.1±0.8 vs 3.1±2.1; p<0.001). One death due to heart failure was observed. The mean LVEF increased from 38% to 42% (p>0.05). Conclusions: Clinical status improvement was observed with low mortality rate in the long-term follow-up. No new regional wall motion abnormalities were observed, and the increase of global ejection fraction was noted.

Angiographic result of index PCI determines the presence of right ventricular infarction in patients with acute inferior myocardial infarction.

It is still a matter of debate which patients with acute inferior myocardial infarction are at increased risk of developing right ventricular (RV) myocardial infarction (RVMI). Cardiac magnetic resonance imaging (CMRI) with late enchancement (LE) is regarded as the gold standard for RVMI assessment. We aimed to determine the impact of initial angiographic status and salutary effect of primary percutaneous coronary intervention (PCI) on the presence of RVMI. In 114 patients undergoing emergency angiography and primary PCI of right coronary artery, 3-5 days after index PCI, LE CMRI was performed for assessing the RVMI. Forty-eight patients (42%) demonstrated RVMI. Multivariate regression analysis identified TIMI flow <2 in at least one RV branch after PCI as an independent angiographic predictor of RVMI [odds ratio (OR) 143.00, 95% confidence interval (CI) 18.10-1130.05, p < 0.001]. ST-segment elevation ≥ 1 mm in V4R was present in 83 (73%). TIMI flow <3 in at least one RV branch before PCI (OR 4.07, 95% CI 1.24-13.33, p = 0.02) was independent angiographic predictor of ST-segment elevation ≥ 1 mm in V4R. The only predictor of RVMI was TIMI flow <2 in at least one RV branch after PCI. ST-segment elevation ≥ 1 mm in V4R is caused by TIMI <3 flow in at least one RV branch before index PCI.

MRI-based evidence for myocardial involvement in women with hypereosinophilic syndrome.

PURPOSE: The aim of the study was to assess the presence and spectrum of cardiac abnormalities identified by cardiac magnetic resonance (CMR) in women with hypereosinophilic syndrome (HES) of undefined etiology, who present with normal electrocardiography (ECG) and transthoracic echocardiography (TTE) and no history of heart disease. METHODS: Ten women (mean age, 48 ± 14 years) with HES of undefined etiology, normal ECG and TTE, and no history of heart disease underwent CMR. RESULTS: CMR showed cardiac abnormalities in 6 subjects. Five patients had nonischemic late gadolinium enhancement (LGE) lesions within the left ventricular (LV) myocardium, and 3 patients demonstrated CMR evidence of myocardial inflammation. The LV ejection fraction was 68.5 ± 5.7%, and the end-diastolic volume index was 62.7 ± 14.7 mL/m(2). The maximum measured blood eosinophil count correlated with LVLGE volume (r = 0.80, P = 0.006) and was 11374 ± 6242 cells/µL and 4114 ± 2972 cells/µL (P = 0.047) in patients with and without LGE lesions, respectively. The actual blood eosinophil count in subjects with and without CMR evidence of myocarditis was 1058 ± 520 cells/µL and 354 ± 377 cells/µL (P = 0.04), respectively. CONCLUSIONS: Despite normal ECG, TTE, and absence of history of heart disease, women with HES of unknown etiology frequently demonstrate cardiac abnormalities on CMR, the presence and extent of which are related to blood eosinophil count.

An unusual cause of bilateral massive peripheral edema in a young male with type 1 diabetes mellitus.

The present article demonstrates an unusual case of bilateral massive peripheral edema caused by neurogenic areflexic bladder in diabetes mellitus type 1. A 28-year-old patient with diabetes type 1 treated for a number of years was referred to the department of internal medicine because of massive edema of his lower limbs. Blood samples revealed increased concentrations of glucose (21.2 mmol/L) and glycated hemoglobin (8.5%). The computed tomography examination of abdomen and pelvis confirmed enlargement of the bladder, with smooth external contour and normal wall thickness. In addition, computed tomography demonstrated bilateral compression of the iliac veins caused by the enlarged bladder. This case highlights the importance of keeping a broad differential diagnosis in mind for patients with diabetes and massive peripheral edema. Neurogenic bladder should be considered in the differential diagnosis, especially for patients with poor glycemia control and long-standing diabetes complicated by diabetic neuropathy.

Feature-tracking cardiovascular magnetic resonance as a novel technique for the assessment of mechanical dyssynchrony.

BACKGROUND: Myocardial tagging using cardiovascular magnetic resonance (CMR) is the gold-standard for the assessment of myocardial mechanics. Feature-tracking cardiovascular magnetic resonance (FT-CMR) has been validated against myocardial tagging. We explore the potential of FT-CMR in the assessment of mechanical dyssynchrony, with reference to patients with cardiomyopathy and healthy controls. METHODS: Healthy controls (n=55, age: 42.9 ± 13 yrs, LVEF: 70 ± 5%, QRS: 88 ± 9 ms) and patients with cardiomyopathy (n=108, age: 64.7 ± 12 yrs, LVEF: 29 ± 6%, QRS: 147 ± 29 ms) underwent FT-CMR for the assessment of the circumferential (CURE) and radial (RURE) uniformity ratio estimate based on myocardial strain (both CURE and RURE: 0 to 1; 1=perfect synchrony) RESULTS: CURE (0.79 ± 0.14 vs. 0.97 ± 0.02) and RURE (0.71 ± 0.14 vs. 0.91 ± 0.04) were lower in patients with cardiomyopathy than in healthy controls (both p<0.0001). CURE (area under the receiver-operator characteristic curve [AUC]: 0.96), RURE (AUC: 0.96) and an average of these (CURE:RUREAVG, AUC: 0.98) had an excellent ability to discriminate between patients with cardiomyopathy and controls (sensitivity 90%; specificity 98% at a cut-off of 0.89). The time taken for semi-automatically tracking myocardial borders was 5.9 ± 1.4 min. CONCLUSION: Dyssynchrony measures derived from FT-CMR, such as CURE and RURE, provide almost absolute discrimination between patients with cardiomyopathy and healthy controls. The rapid acquisition of these measures, which does not require specialized CMR sequences, has potential for the assessment of mechanical dyssynchrony in clinical practice.

Left ventricular mass is preserved in patients with idiopathic pulmonary arterial hypertension and Eisenmenger's syndrome.

BACKGROUND: Left ventricular (LV) atrophic remodelling was described for chronic thromboembolic pulmonary hypertension (PH) but not in other forms of PH. We aimed to assess LV morphometric changes in idiopathic pulmonary arterial hypertension (IPAH) and Eisenmenger's syndrome(ES). METHODS: Fifteen patients with IPAH, 15 patients with ES and 15 healthy volunteers were included. Magnetic resonance was used to measure masses of LV, interventricular septum (IVS), LV free wall (LVFW), and LV end diastolic volume (LVEDV) indexed for body surface area. RESULTS: Between patients with IPAH, ES and controls no differences in LVmassindex (54.4[45.2-63.3] vs 58.7[41.5-106.1] vs 52.8[46.5-59.3], p=0.50), IVSmassindex (21.6[18.2-21.9)] vs 27.4[18.0-32.9] vs 20.7[18.2-23.2], p=0.18), and LVFWmassindex ([32.4[27.1-40.0] vs 36.7[30.9-62.1] vs 32.5[26.9-36.1], p=0.29) were found. LVEDVindex was lower in IPAH patients than in controls and in ES patients (54.9[46.9-58.5] vs 75.2[62.4-88.9] vs 73.5[62.1-77.5], p<0.001). In IPAH LVEDV but not LV mass correlated with pulmonary vascular resistance (r=-0.56, p=0.03) and cardiac output (r=0.59, p=0.02). CONCLUSIONS: LV mass is not reduced in patients with IPAH and with ES and is not affected by haemodynamic severity of PH. LVEDV is reduced in IPAH patients in proportion to reduced pulmonary flow but preserved in patients with ES, where reduced pulmonary flow to LV is compensated by right-to left shunt.

Computed tomography characteristics of coronary artery atherosclerosis in subjects with lower extremity peripheral artery disease and no cardiac symptoms.

INTRODUCTION:  Computed tomography coronary angiography (CTCA) enables noninvasive evaluation of coronary artery atherosclerosis. However, its value to assess coronary artery disease (CAD) in subjects with lower­extremity peripheral artery disease (PAD) and no cardiac symptoms is unknown. Moreover, the relationship between coronary artery plaque characteristics and severity of peripheral atherosclerosis in this group of patients was not sufficiently elucidated. OBJECTIVES:  The aim of the study was to determine the value of CTCA to assess coronary artery atherosclerosis and to evaluate the relationship between coronary artery plaque characteristics and severity of peripheral atherosclerosis in subjects with lower­extremity PAD and no cardiac symptoms. PATIENTS AND METHODS:  Sixty­five individuals (45 men, 20 women, mean age, 62.5 ±7.6 years) with lower­extremity PAD and no cardiac symptoms underwent CTCA. RESULTS:  CTCA revealed CAD in 56 subjects. Twenty­two had obstructive CAD. The mean ankle-brachial index (ABI) was 0.64 ±0.16. Twenty­six individuals demonstrated abnormal carotid artery intima-media thickness (IMT). ABI lower than median, if compared with ABI equal of higher than median, was associated with a higher proportion of obstructive multivessel to single vessel CAD (8:4 vs. 1:9; P = 0.01) and higher number of coronary artery segments with mixed plaques (2.3 ±2.2 vs. 1.2 ±1.3; P = 0.02). Comparing patients with abnormal and normal IMT, the former demonstrated higher proportion of obstructive multivessel to single-vessel CAD (7:3 vs. 2:10; P = 0.01) and higher number of coronary artery segments with noncalcified (1.9 ±3.2 vs. 0.6 ±1.4; P = 0.04) and mixed plaques (2.3 ±2.1 vs. 1.3 ±1.7; P = 0.049). CONCLUSIONS:  CTCA may be effective to detect CAD in subjects with lower­extremity PAD and no cardiac symptoms. The low ABI and abnormal IMT are associated with more extensive CAD and higher burden of high­risk coronary artery plaques.