Radoslaw Piatkowski

Baseline platelet size is increased in patients with acute coronary syndromes developing early stent thrombosis and predicts future residual platelet reactivity. A case-control study

INTRODUCTION Pre-procedural predictors of early stent thrombosis (ST) and future response to platelet inhibitors are in demand. We sought to evaluate the impact of baseline platelet indices on the occurrence of early ST and future residual platelet reactivity. MATERIALS AND METHODS Hundred and eight patients with acute coronary syndromes (ACS) in whom stents were implanted were included: 36 consecutive ST cases and 72 matched controls. Platelet indices assessed with flow cytometry before stent implantation were retrieved from the departments data base. Residual platelet reactivity specific to aspirin (aspirin reaction units-ARU) and clopidogrel (P2Y12 reaction units-PRU) was assessed prospectively with VerifyNow under dual antiplatelet treatment. RESULTS Platelet size reported as mean platelet volume (MPV) or proportion of large platelets (LPLT) was significantly higher in ST cases compared with controls (10.4, 95% confidence intervals [CI], 10.1-10.8 vs. 9.7, CI, 9.5-9.9, P=0.0004 and 35.8, CI, 34.2-37.3 vs. 33.3, CI, 32.2-34.3, P=0.007, respectively). Dual aspirin and clopidogrel poor-responsiveness was diagnosed significantly more often in ST cases than in controls (19.6% vs. 1.4%, P=0.004), whereas no difference was observed for single aspirin or clopidogrel poor-responsiveness. A strong correlation was found between MPV and both, ARU (r=0.66, P<0.0001) and PRU (r=0.55, P<0.0001). Similarly, higher LPLT was associated with higher ARU (r=0.47, P<0.0001) and PRU (r=0.38, P=0.0001). CONCLUSIONS Baseline platelet size is increased in patients with ACS developing early ST and correlates with future residual platelet reactivity under aspirin and clopidogrel therapy. Dual but not isolated aspirin or clopidogrel poor-responsiveness appears to be associated with early ST.

Simple markers can distinguish Takotsubo cardiomyopathy from ST segment elevation myocardial infarction

BACKGROUND Takotsubo cardiomyopathy (TTC) is a clinical condition mimicking acute myocardial infarction. A specific biomarker for TTC screening is required, but until now, no single biomarker has been established for the early diagnosis of TTC and differentiation from ST-segment elevation myocardial infarction (STEMI). In our study we focused on the simple markers that are available in every hospital. METHODS In 66 consecutive patients (pts) who were hospitalized with TTC and 66 pts with STEMI, cardiac biomarkers, such as NT-proBNP, TnI, CK and CKMB mass were determined during 12h from admission and compared with demographic, clinical and echocardiographic findings. RESULTS The concentration of NTproBNP was greater in pts with TTC than STEMI (4702pg/ml vs 2138pg/ml). The concentration of TnI and CKMB mass was greater in the STEMI group than in the TTC group (TnI: 2.1ng/ml and CK MB mass: 9.5ng/ml in pts with TTC vs TnI: 19ng/ml and CK MB mass: 73.3ng/ml in pts with STEMI). The NTproBNP/TnI ratio and NTproBNP/CKMB mass ratio were, respectively, 2235.2 and 678.2 in pts with TTC and 81.6 and 27.5 in pts with STEMI (p<0.001). Moreover, the NTproBNP/EF ratio was also statistically significant (110.4 in TTC group and 39.4 in STEMI group). CONCLUSIONS NTproBNP/TnI, NTproBNP/CKMB mass and NTproBNP/EF ratios can distinguish TTC from STEMI at an early stadium. The most accurate marker is the NTproBNP/TnI ratio.

The oldest patient with takotsubo cardiomyopathy

Takotsubo cardiomyopathy (TTC) is a rare condition that affects mainly aging women. According to a retrospective review, patients with TTC accounted for approximately 2% of all the patients with suspected acute coronary syndrome (ACS). A few reports indicated that the average age of TTC patients was 68 years, although children or young adults may also be affected. In US and Europe, a number of contemporary TTC studies report that 90% of patients with TTC are women aged 65–70 years. Meta analysis showed that the age ranged from 10 to 89 years. [1] There was also one case study of a 90-year-old patient with TTC ― the oldest patient known so far. In that case, the patient died during the course of treatment from severe multi-organ failure. [2] In the present case report, we present a 98-years old woman with TTC admitted to our clinic. A 98-years old patient was admitted to our clinic because of significant chest pain and general weakness accompanied by hypotension that required catecholamine administration with ST-segment elevation in the anterolateral leads in ECG. The patient suffered from hypertension and third stage of chronic kidney disease. Urgent cardiac catheterization and ventriculography confirmed the absence of any critical coronary disease, but also the presence of a typical apical ballooning and midventricular hypokinesis. Troponin I (TnI) at admission was 5.555 ng/mL and creatine kinase soenzyme MB (CK-MB) mass was 14.5 ng/mL. Inflammatory parameters were not elevated, whereas N-terminal pro brain natriuretic peptide (NT-proBNP) concentration was markedly elevated, at 18,623 pg/mL. NT-proBNP/TnI ratio was 3352.48 on the first day and even higher after 24 h, at 7113.36. This markers profile is characteristic of TTC. There is a relatively small increase in creatine kinase and troponin concentrations in relation to the extent of wall motion abnormalities. BNP is always elevated in patients with TTC and is higher than in patients with ST-segment elevation myocardial infarction. Some researchers suggest that TTC can be distinguished from ACS on the basis of the characteristic profile of cardiac markers consisting of a sudden increase in the concentration of NT-proBNP in the first few days when there is only a small increase in markers of myocardial necrosis (the ratio of NT-pro BNP/troponin). [3]

Transoesophageal real-time three-dimensional echocardiography in assessing large multiperforated atrial septal aneurysm

A 51-year-old woman presented with a 2 year history of declining exercise capacity and irregular palpitations. Clinical examination revealed sinus rhythm at 86 b.p.m., and blood pressure of 112/70 mmHg, without pedal oedema. Initial transthoracic echocardiography (TTE) revealed moderate right ventricular (RV) enlargement with moderate tricuspid regurgitation and mild pulmonary hypertension (estimated PASP 40 mmHg). There was interventricular septal flattening in diastole due to RV volume overload. Transoesophageal two-dimensional echocardiography (2D TEE) demonstrated multiperforated atrial septal aneurysm (ASD II-atrial septal defects type II) …

Usefulness of Live/Real Time Three‐Dimensional Transesophageal Echocardiography in the Assessment of Severe Mitral Annuloplasty Ring Dehiscence

A 47-year-old patient was presented with a 2-month history of progressive dyspnea (New York Heart Association IV). He had a history of myocardial-infarction-treated percutaneous coronary angioplasty of the culprit lesion in the left anterior descending artery with implantation of a bare-metal stent complicated by late stent thrombosis and heart failure. One year later, the patient had undergone restrictive mitral annuloplasty using small (23 mm), complete ring because of severe ischemic mitral regurgitation. Clinical examination revealed sinus rhythm at 80 beats/min and blood pressure of 112/70 mmHg, apical holosystolic blowing murmur, and bibasilar crackles. Two-dimensional transesophageal echocardiography (2D TEE) revealed a dilated left ventricle and severe paraannular mitral regurgitation, as well as significant tricuspid regurgitation (Fig. 1A, B). Three-dimensional TEE (3D TEE) revealed an extensive inferolateral dehiscence (Fig. 1C, movie clip S1) of the mitral annuloplasty ring, dilated mitral annulus, and severe (vena contracta area (VCA)—1.35 cm2) eccentric paraannular inferoposterolaterally directed jet (Fig. 1D, movie clip S2) (Fig. 2). The patient underwent an urgent successful mitral valve replacement with mechanical valve and tricuspid annuloplasty.

Dislocation of Amplatzer Septal Occluder Device after Closure of Secundum Atrial Septal Defect

Atrial septal defect transcatheter occlusion techniques have become an alternative to surgical procedures. With the increasing use of this new technology, several complications have been identified. The authors present the case of a patient who was admitted to the hospital for primary percutaneous closure of a secundum atrial septal defect. On routine follow-up examination 24 hours after implantation, transthoracic echocardiography revealed a partial dislocation of the occluder into the right atrium. The patient was referred for cardiosurgical treatment. Strict selection criteria and the choice of the device may help reduce the incidence of complications such as dislocation of the occluder into the right atrium following the percutaneous device closure of an atrial septal defect.

Purulent pericarditis in patient with esophageal cancer presenting with cardiac tamponade.

A 39-year-old patient with no relevant history of cardiovascular disease presented after syncope, with rest dyspnea and no chest pain. A few months earlier, the patient had undergone palliative stent implantation in the distal part of the esophagus due to inoperable esophageal cancer. On admission, physical examination of the patient revealed the following: cachexia with severe dehydration, arterial hypotension (90/50 mm Hg), tachycardia (heart rate 115 beats/min), tachypnea (36 breaths/min), body temperature of 37°C (98.6°F), distended neck veins, no pulmonary congestion, mild hepatomegaly, and decreased heart sounds. The initial electrocardiogram (ECG) showed persistent diffuse concave-upward ST-segment elevation that was not confined to any arterial territory (Figure 1). The baseline serum troponin I level was not elevated. Bedside transthoracic echocardiography (TTE) demonstrated a considerable (about 5 cm) amount of heterogeneous fluid in the pericardium with numerous non-regular, mobile fibrin clots creating thin intrapericardial bands (Figure 2a). In addition, TTE showed various signs indicating cardiac tamponade (near total diastolic collapse of the right ventricle and the right atrium; excess buildup of fluid in the vena cava, known as inferior vena cava [IVC] plethora; the absence of normal inspiratory IVC collapse; and respiratory variations in tricuspid and transmitral flow on Doppler echocardiography) (Figures 2b–d). Emergency pericardio-

Are normal coronary arteries a typical feature of apical ballooning syndrome

Apical ballooning syndrome (ABS) is a new and uncommon, yet very interesting, clinical phenomenon regarded as one of the important elements of differential diagnosis in acute myocardial infarction. It was first described in 1990. The absence of obstructive coronary artery disease among others is a typical feature of ABS, required to make a final diagnosis. We describe a case of a woman with ultrasonographically confirmed tight stenosis in the right coronary artery, yet showing all other characteristics of ABS.

Complication of Acute Myocardial Infarction by Systemic Arterial Embolism in the Era of Multimodality Imaging

A 51-year-old man with a history of smoking was admitted to the hospital with anterolateral myocardial infarction within 3 h after the onset of symptoms. Coronary angioplasty of the total occlusion of the proximal left anterior descending artery was performed with implantation of a bare-metal stent. The patient received typical pharmacological treatment, including 300 mg of acetylsalicylic acid, 600 mg of clopidogrel, 5000 units of unfractionated heparin, and a continuous intravenous infusion of abciximab. Echocardiography, performed the day after admission, showed akinesis within the anterior wall, the interventricular septum, and the apex of the left ventricle (ejection fraction = 45%) (Figure 1A). Contrast echocardiography did not reveal intraventricular thrombus (Figure 1B, Video 1). On the 6th day of hospitalization, the patient complained of right-hand paresthesia. On physical examination, the hand was pale and cold, with no pulse palpable over the right radial and ulnar arteries. Computed tomography angiography disclosed embolism at the right brachial artery bifurcation