Adam Mazurek

Myocardial regeneration strategy using Wharton's jelly mesenchymal stem cells as an off-the-shelf 'unlimited' therapeutic agent: results from the Acute Myocardial Infarction First-in-Man Study.

Introduction In large-animal acute myocardial infarction (AMI) models, Whartons jelly (umbilical cord matrix) mesenchymal stem cells (WJMSCs) effectively promote angiogenesis and drive functional myocardial regeneration. Human data are lacking. Aim To evaluate the feasibility and safety of a novel myocardial regeneration strategy using human WJMSCs as a unique, allogenic but immuno-privileged, off-the-shelf cellular therapeutic agent. Material and methods The inclusion criterion was first, large (LVEF ≤ 45%, CK-MB > 100 U/l) AMI with successful infarct-related artery primary percutaneous coronary intervention reperfusion (TIMI ≥ 2). Ten consecutive patients (age 32–65 years, peak hs-troponin T 17.3 ±9.1 ng/ml and peak CK-MB 533 ±89 U/l, sustained echo LVEF reduction to 37.6 ±2.6%, cMRI LVEF 40.3 ±2.7% and infarct size 20.1 ±2.8%) were enrolled. Results 30 × 106 WJMSCs were administered (LAD/Cx/RCA in 6/3/1) per protocol at ≈ 5–7 days using a cell delivery-dedicated, coronary-non-occlusive method. No clinical symptoms or ECG signs of myocardial ischemia occurred. There was no epicardial flow or myocardial perfusion impairment (TIMI-3 in all; cTFC 45 ±8 vs. 44 ±9, p = 0.51), and no patient showed hs-troponin T elevation (0.92 ±0.29 ≤ 24 h before vs. 0.89 ±0.28 ≤ 24 h after; decrease, p = 0.04). One subject experienced, 2 days after cell transfer, a transient temperature rise (38.9°C); this was reactive to paracetamol with no sequel. No other adverse events and no significant arrhythmias (ECG Holter) occurred. Up to 12 months there was one new, non-index territory lethal AMI but no adverse events that might be attributable to WJMSC treatment. Conclusions This study demonstrated the feasibility and procedural safety of WJMSC use as off-the-shelf cellular therapy in human AMI and suggested further clinical safety of WJMSC cardiac transfer, providing a basis for randomized placebo-controlled endpoint-powered evaluation.

Myocardial Ischaemia, Coronary Atherosclerosis and Pulmonary Pressure Elevation in Antiphospholipid Syndrome Patients

BACKGROUND Thrombotic events in antiphospholipid syndrome (APS) involve venous and arterial circulation with the possible involvement of coronary or pulmonary microcirculation. OBJECTIVES To evaluate the influence of antiphospholipid antibodies (aPL) and on myocardial ischaemia assessed by single-photon emission computerized tomography (SPECT), coronary atherosclerosis assessed by multidetector computerized tomography (MDCT) and pulmonary pressure assessed by transthoracic echocardiography (TTE) in patients with primary antiphospholipid syndrome (PAPS). MATERIAL AND METHODS TTE, SPECT (Tc 99m sestamibi) and MDCT-based coronary calcium scoring were performed in 26 consecutive PAPS patients (20 females, 6 males, aged 20-61, mean 39.7) without any signs of other autoimmunological disease and without clinical symptoms of heart disease. RESULTS Out of 26 patients, TEE showed normal left and right ventricle function in 25 (96.2%) and elevated (≥ 30 mm Hg) right ventricle systolic pressure in 7 (26.9%) patients. SPECT revealed myocardial perfusion defects in 15 (57.7%) patients: exercise-induced in 6 (23.1%) and persistent in 11 (42.3%). MDCT revealed coronary calcifications in 4 (15.4%) patients. The number of plaques ranged from 1 to 11 (median 2), volume 3-201.7 mm³ (median 7), calcium scores 1.3-202.6 (median 5.7). In the group with perfusion defects or coronary calcifications (n = 15), all the patients showed elevated aCL IgG. CONCLUSIONS In most of the relatively young APS patients, without any symptoms of ischemic heart disease, SPECT showed myocardial perfusion defects, and coronary calcifications in 1/6 of them. Right ventricle systolic pressure was elevated in 1/4 of APS patients. These pathologies, well known as cardiovascular risk markers, were associated with elevated levels of the IgG class of both anti-cardiolipin and antiB2 GPI antibodies. Thus, in a high percentage of APS patients, clinically silent myocardial ischaemia, pulmonary pressure elevation and coronary atherosclerosis are present and related to the presence of antiphospholipid antibodies.

Myocardial infarction in Fabry disease – misfortune or companion? Case report and review of the literature (RCD code: III‑3B.2)

We discuss a 56‑year‑old man with Fabry disease (FD), a genetic X‑linked glycolipid storage disorder. The patient presented at the Emergency Room in a local hospital due to tachycardia‑associated chest pain, which had occurred occasionally in the past, but on that occasion was long‑lasting (>12h) and distressing. The patient had been diagnosed with FD at the age of 42. He presented a range of symptoms characteristic for the condition, including hypertrophic cardiac myopathy with impaired left ventricular relaxation, angiokeratomas, cornea verticillata, hypohydrosis and acroparesthesia. Residual alpha‑galactosidase A activity at diagnosis was ≈3%. The Enzyme Replacement Therapy (ERT) with the agalsidase alpha was induced. A year later pacemaker implantation was performed due to sick sinus syndrome with symptomatic, severe episodes of bradycardia. The initial diagnosis was tachycardia‑associated chest pain with troponin release in the context of FD left ventricular hypertrophy. However, a decision was made to perform an urgent angiographic evaluation to exclude coronary pathology as a potential factor in the clinical picture. Coronary angiography showed a critical, flow-limiting, stenosis of the left anterior descending artery (LAD) which changed the initial type 2 myocardial infarction (MI) diagnosis to the type 1 MI. Percutaneous stent‑assisted treatment was performed with an optimal angiographic and clinical outcome. However, 5 days later the patient developed a minor left hemispheric ischaemic stroke. In conclusion, the clinical course of a rare pathology such as FD may be importantly complicated by other (more common) pathologies. Physicians, in their diagnostic and therapeutic decision‑making, need to be open to thinking beyond the patient label. JRCD 2018; 3 (7): 246–252

TCT-796 Highly Calcific Carotid Lesions Endovascular Revascularization Using a Novel, Dual-layer Carotid Stent System CGuardTM: Analysis from the PARADIGM Study

TCT-796 Highly Calcific Carotid Lesions Endovascular Revascularization Using a Novel, Dual-layer Carotid Stent System CGuardTM: Analysis from the PARADIGM Study Adam Mazurek, Mariusz Trystuła, Jacek Jąkała, Andrzej Brzychczy, Anna Borraty nska, Agata Le sniak-Sobelga, Małgorzata Urba nczyk, R. Paweł Bany s, Wojciech Zajdel, Klaudia Proniewska, Lukasz Partyka, Krzysztof Zmudka, Piotr Podolec, Piotr Musialek Department od Cardiac and Vascular Diseases, John Paul II ND Hospital, Krakow, Poland; School of Medicine, University of California, Irvine; UC Davis; Kurume-univaersity; John Paul II Hospital, Krakow, Poland; Al Qassimi Hospital; Clinical centre of Serbia; John Paul II Hospital, Krakow, Poland; Clinical Dept. of Interventional Cardiology, John Paul II Hospital, Krakow, Poland; Krakow Cardiovascular Research Institute, Krakow, Poland; University Hospital Krakow, Krakow, Poland; John Paul II Hospital in Krakow, Krakow, Poland; Clinical Center of Serbia; John Paul II Hospital, Krakow, Poland