Monika Komar

The benefit of atrial septal defect closure in elderly patients

Objective Closure of an atrial septal defect in elderly patients is controversial. The aim of the study was to evaluate the outcomes of transcatheter closure of secundum atrial septal defects (ASDs) in elderly patients. Patients and methods From a total of 488 patients with ASDs who underwent transcatheter closure, 75 patients aged over 60 years (45 female, 30 male) with a mean age of 65.3±15.7 (60–75) years were analyzed. All patients had an isolated secundum ASD with a mean pulmonary blood flow:systemic blood flow of 2.84±1.9 (1.5–3.9). Symptom-limited treadmill exercise tests with respiratory gas-exchange analysis and transthoracic color Doppler echocardiographic study, as well as quality of life measured using the Short Form (36) Health Survey (SF-36) were repeated in all patients before the procedure and after 12 months of follow-up. Results The atrial septal device was successfully implanted in all patients (procedure time 37.7±4.5 [13–59] minutes, fluoroscopy time 11.2±9.9 [6–40] minutes). There were no major complications. The defect echo diameter was 17.7±15.8 (12–30) mm. The mean balloon-stretched diameter of ASDs was 22.4±7.9 (14–34) mm. The diameter of the implanted devices ranged from 16 to 34 mm. Significant improvement of exercise capacity was noted at 6 and 12 months after the procedure. Exercise time within 6 months of ASD closure was longer (P<0.001) compared to baseline values, and also oxygen consumption increased (P<0.001). Seven quality-of-life parameters (except mental health) improved at 12-month follow-up compared to baseline data. The mean SF-36 scale increased significantly in 66 (88%) patients, with a mean of 46.2±19.1 (5–69). As early as 1 month after the procedure, a significant decrease of the right ventricular dimension and the right atrium dimension was observed (P<0.001). The right ventricular dimension decreased in 67 patients (89.3%). Conclusion Closure of ASDs in elderly patients caused significant clinical and hemodynamic improvement after percutaneous treatment, which was maintained during long-term follow-up, justifying this procedure in old age.

Assessment of left ventricle function in patients with symptomatic and asymptomatic aortic stenosis by 2-dimensional speckle-tracking imaging

Summary Background Global longitudinal peak strain (GLPS) quantifies left ventricle (LV) long-axis contractility. Early detection of LV systolic dysfunction is pivotal in diagnosis and treatment of patients with aortic stenosis (AS). This study was performed to assess LV longitudinal systolic function by GLPS derived from 2-dimensional speckle tracking imaging (2D-STI) in AS patients in comparison to standard echocardiographic parameters. Material/Methods Laboratory tests, standard echocardiography, tissue Doppler imaging (TDI) and 2D-STI examinations with GLPS calculation were performed in 49 consecutive patients with moderate to severe AS with LV ejection fraction ≥50% and 18 controls. Results While LVEF do not differentiate AS patients from controls, GLPS was significantly decreased in the AS group (−15.30±3.25% vs. −19.60±2.46% in controls, p<0.001). GLPS was significantly reduced in symptomatic AS patients as compared to the asymptomatic AS group [−15.5 (11.8–16.8) vs. −17.5 (14.7–18.9)%, p=0.02]. Conclusions In aortic stenosis patients, despite normal left ventricle ejection fraction, long-axis left ventricular function is impaired, which manifests in global longitudinal peak strain reduction. GLPS reveals that LV function impairment is more pronounced in symptomatic as compared to asymptomatic AS patients. Further studies are needed to determine the prognostic significance of early LV function impairment in aortic stenosis patients showed by GLPS.

Aspirin resistance in adult patients after Fontan surgery

BACKGROUND Thrombotic complications are common in adult patients who have had a Fontan operation early in life for treatment of congenital heart disease. OBJECTIVE To characterize platelet function and responsiveness to aspirin in relation to thrombogenesis, systemic inflammation, and markers of endothelial function in adults with Fontan circulation (FC). METHODS Thirty-four FC patients (age 18-40years; 62% taking aspirin chronically and 38% not taking aspirin) and 32 age- and sex-matched healthy controls were studied. Platelet function was evaluated by measurement of basal concentrations of thromboxane B2 (TXB2) and sCD40L and ex-vivo generation of TXB2 and sCD40L. Plasma concentrations of thrombin-antithrombin, endothelin-1, vWF, IL-6, IL-8, MCP-1, MIP-1β, TNFα, sVCAM-1, and syndecan-1 also were measured. RESULTS Platelet numbers were significantly lower in FC patients than in controls, but the patients had significantly higher platelet activity, as evidenced by higher TXB2 and sCD40L concentrations and higher ex vivo generation of TXB2. Chronic aspirin treatment had no effect on plasma concentrations of TXB2 and sCD40L in FC, but in 52% of aspirin-treated FC subjects, TXB2 concentrations remained elevated at 60min of TXB2 generation, indicating aspirin resistance. In addition, FC patients had increased levels of thrombin-antithrombin, endothelin-1, vWF, IL-8, MCP-1, MIP-1β, TNFα, sVCAM-1, and syndecan-1 but not of IL-6. CONCLUSION Adults with FC had lower platelet numbers but increased platelet activity, increased thrombogenesis, systemic inflammation, and endothelial dysfunction. A significant proportion of aspirin-treated FC adults had aspirin resistance, which may be at least in part responsible for their increased incidence of thrombotic complications.

Is it worth closing the atrial septal defect in patients with insignificant shunt

Introduction Closure of the atrial septal defect in patients with insignificant shunt is controversial. Aim To evaluate the outcomes of transcatheter closure of atrial septal defect (ASD) in symptomatic patients with borderline shunt. Material and methods One hundred and sixty patients (120 female, 40 male) with a mean age of 30.1 ±16.2 (20–52) years with a small ASD who underwent transcatheter closure were analyzed. All patients had a small ASD with Qp: Qs ratio ≤ 1.5, mean 1.2 ±0.9 (1.1–1.5) in echo examination. Cardiopulmonary exercise tests, clinical study, transthoracic echocardiographic study as well as quality of life (QoL) (measured using the SF36 questionnaire (SF36q)) were repeated in all patients before and after the procedure. Results The devices were successfully implanted in all patients. After 12 months of ASD closure, all the patients showed a significant improvement of exercise capacity (oxygen consumption – 21.9 ±3.1 vs. 30.4 ±7.7, p > 0.001). The QoL improved in 7 parameters at 12-month follow-up. The mean SF36q scale increased significantly in 141 (88.1%) patients of mean 43.2 ±20.1 (7–69). A significant decrease of the right ventricular area (20.3 ±1.3 cm2 vs. 18.3 ±1.2 cm2, p < 0.001) and the right atrial area (15.2 ±1.9 cm2 vs. 12.0 ±1.6 cm2, p < 0.001) was observed at 12-month follow-up. Conclusions Closure of ASD in the patients with insignificant shunt resulted in significant durable clinical and hemodynamic improvement after percutaneous treatment.

Improvement of physical capacity in patients undergoing transcatheter closure of atrial septal defects

Introduction Atrial septal defect (ASD) is the most common congenital cardiac anomaly diagnosed in adults. It often remains asymptomatic until the fourth or fifth decade of life. Significant left-to-right interatrial shunting is associated with the risk of heart failure, pulmonary hypertension and atrial fibrillation. Percutaneous ASD closure is a recognized method of treatment. Aim To evaluate the clinical outcomes and physical capacity in patients undergoing transcatheter closure of ostium secundum ASD. Material and methods One hundred and twenty adult patients (75 females and 45 males) with a mean age of 43.1 ±13.3 (17–78) years who underwent transcatheter device closure of ostium secundum ASD were analyzed. Clinical evaluation and transthoracic color Doppler echocardiographic study were repeated in all patients before as well as 1 and 24 months after the procedure. To assess the physical capacity symptom-limited treadmill exercise tests with respiratory gas-exchange analysis were performed in all patients before the procedure and after 24 months of follow-up. Results The devices were successfully implanted in all patients. During 24 months of follow-up all patients showed significant clinical and spiroergometric improvement of exercise capacity, and a significant decrease of right heart chamber overload features on echocardiography. Conclusions Transcatheter closure of ASD in patients with significant shunt resulted in significant clinical and hemodynamic improvement regardless of the baseline functional class.

Spontaneous dislocation of the endocardial lead into the left ventricle through the intraventricular septum

We report a case of a 66-year-old woman with a history of DDD pacemaker implantation in 2005 due to vasovagal syncope and generator change in 2014. The patient was implanted with an atrial lead Biotronik SX 53-JBP positioned in the right atrial appendage and a ventricular lead Biotronik SX 60-BP positioned in the right ventricular apex. A few months after generator change the patient underwent a diagnostic process due to heart palpitations and stabbing pain in the chest. The chest pain occurred during body movements and deep breathing. In electrocardiographic Holter monitoring the sensing disturbances in the ventricular channel were detected. During pacemaker interrogation the electrical parameters of both leads were normal except for an increased number of short V-V intervals. The patient was qualified to transvenous ventricular lead extraction and implantation of a new ventricular lead. In the meantime the patient underwent a computed tomography scan in search of coronary heart disease, and it was found that the ventricular lead was perforating the intraventricular septum on the level of the apical septal segment. The length of the lead in the left ventricle amounted to 7–9 mm (Fig. 1A). The displacement of the lead was suspected also in a chest X-ray of the current location of the lead (Fig. 1B). In transthoracic and transoesophageal echocardiography the thrombus on the lead tip and left-to-right shunt through the septum along the lead were ruled out (Fig. 1C). The decision to extract the ventricular lead transvenously with mechanical systems with surgical backup and transoesophageal echocardiography monitoring was upheld. The procedure was a complete success. There was no residual left-to-right shunt after the extraction of the lead. Subsequently the new ventricular lead was implanted (Fig. 1D). The presented case is an example of a rare and dangerous complication of permanent pacing. The existence of a short portion of ventricular lead inside the left ventricle posed a risk of thrombus formation and peripheral embolisation, of which the most dangerous is stroke. The late perforation of intraventricular septum by a passive fixation lead has not been reported in English-language literature yet. The probable cause of the distant (in time) perforation was the application of excessive force on the tip of the lead during implantation, which was then aggravated by the ingrown lead into the tricuspid valve region. Transvenous extraction of the lead displaced into the left ventricle requires surgical intervention according to the current Heart Rhythm Society (HRS) expert consensus. In this case a less invasive approach was successfully used. However, close attention was directed toward identification and prevention of potential perioperative complications such as left-to-right shunt after lead extraction and arterial embolisation. Furthermore, the procedure was conducted with surgical backup and continuous intraoperative transoesophageal monitoring.

Polish Forum for Prevention Guidelines on Cardiovascular Risk Assessment: update 2016

1Department of Cardiac and Vascular Diseases, Institute of Cardiology, Jagiellonian University Medical College, John Paul II Hospital, Krakow, Poland 21st Department of Cardiology and Hypertension, Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland 3Department of Hypertension and Diabetology, Medical University in Gdansk, Gdansk, Poland 4Department of Clinical Epidemiology and Population Studies, Institute of Public Health, Jagiellonian University Medical College, Krakow, Poland 5Department of Epidemiology, Cardiovascular Disease Prevention and Health Promotion, Institute of Cardiology, Warsaw, Poland 6Department of Haemodynamics and Angiocardiography, John Paul II Hospital, Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland 7Department of Metabolic Diseases, Jagiellonian University Medical College, Krakow, Poland 8Department of Biochemistry and Pharmacogenomics, Division of Biochemistry and Clinical Chemistry, Medical University of Warsaw, Warsaw, Poland 9Department of Paediatric Cardiology and Rheumatology, Medical University of Lodz, Lodz, Poland 102nd Department of Neurology, Institute of Psychiatry and Neurology, Warsaw, Poland 11Department of Experimental and Clinical Pharmacology, Medical University of Warsaw, Warsaw, Poland 12Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland 13Department of Family Medicine, Jagiellonian University Medical College, Krakow, Poland 14Department of Congenital Heart Disease, Institute of Cardiology, Warsaw, Poland

Wytyczne Polskiego Forum Profilaktyki Chorób Układu Krążenia dotyczące farmakoterapii prewencyjnej: aktualizacja 2017

1Department of Cardiac and Vascular Diseases, Institute of Cardiology, Jagiellonian University Medical College at John Paul II Hospital, Krakow, Poland 21st Department of Cardiology, Medical University of Warsaw, Warsaw, Poland 3Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland 4Chair of Epidemiology and Population Studies, Institute of Public Health, Faculty of Health Sciences, Jagiellonian University Medical College, Krakow, Poland 5Centre for Family and Community Medicine, Faculty of Health Sciences, Medical University of Lodz, Lodz, Poland 6Department of Epidemiology, CVD Prevention, and Health Promotion, Institute of Cardiology, Warsaw, Poland 7Department of Preventive Medicine and Medical Education, Medical University in Gdansk, Gdansk, Poland 81st Department of Cardiology, Interventional Electrocardiology and Hypertension, Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland 9Department of Haemodynamics and Angiocardiography, John Paul II Hospital, Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland 10Department of Metabolic Diseases, Jagiellonian University Medical College, Krakow, Poland 11Department of Pharmacogenomics, Division of Biochemistry and Clinical Chemistry, Medical University of Warsaw, Warsaw, Poland 122nd Department of Neurology, Institute of Psychiatry and Neurology, Warsaw, Poland 13Department of Experimental and Clinical Pharmacology, Medical University of Warsaw, Warsaw, Poland 14Department of Paediatric Cardiology and Rheumatology, Medical University of Lodz, Lodz, Poland 15Department of Family Medicine, Jagiellonian University Medical College, Krakow, Poland 16Department of Internal Diseases and Rural Medicine, Jagiellonian University Medical College, Krakow, Poland

Clinical response to calcium channel blockers in a hemodynamically unstable patient with reactive idiopathic pulmonary arterial hypertension

Acute vasoreactivity testing is indicated in patients with idiopathic pulmonary arterial hypertension (IPAH) to identify subjects who will respond favorably to long-term treatment with calcium channel blockers (CCB) [1]. The result of the test determines the choice of treatment and predicts survival of the patient [2, 3]. It has been suggested that molecular etiology of IPAH is different in patients who respond or do not respond to CCB treatment [4]. In the current guidelines [1, 5] acute va-soreactivity testing is recommended in all patients with IPAH but treatment with CCB is advised only in those in World Health Organization functional class (WHO-FC) I–III. No guidelines are provided for patients with positive acute vasoreactivity testing who are in WHO-FC IV or who are hemodynamically unstable. We present a case of a 29-year-old woman who was urgently admitted to the reference center for pulmonary hypertension from her local hospital due to rapidly progressing dyspnea and recurrent episodes of syncope. Her symptoms started 2 months before and progressed to WHO-FC IV at the time of admission. She presented with resting dyspnea, blood pressure of 90/60 mm Hg, a heart rate of 85 beats per minute and arterial blood saturation of 95%. The electrocardiogram showed sinus rhythm with an incomplete right bundle branch block. Echocardiography showed typical signs of precapillary pulmonary hypertension with right ventricular dysfunction (Table I). N-terminal pro b-type natriuretic pep-tide (NT-proBNP) was significantly elevated (Table I). On the first day of hospitalization the patient experienced syncope after minimal exertion. It was followed by prolonged hypotension which required management with intravenous fluid and continuous infusion of dobutamine. After hemodynamic stabilization, still on dobutamine, she underwent further diagnostic tests according to the current guidelines [1]. She was HIV negative ; pulmonary function tests and lung perfusion scans were normal. Abdominal USG and laboratory tests excluded liver disease. Physical examination and laboratory tests did not suggest a diagnosis of connective tissue disease. Echocardiography was negative for congenital heart disease. These results together with right heart catheterization (day 4) confirmed the diagnosis of IPAH (Table I) [6]. Acute pulmonary vasoreactivity (20 ppm of nitric oxide over 5 min) was positive. Mean pulmonary artery pressure decreased from 49 mm Hg to 26 mm Hg without a change in the cardiac index (2.1 l/min/m 2). We started treatment with amlodipine

Transcatheter closure of atrial septal communication: impact on P-wave dispersion, duration and arrhythmia in mid-term follow-up

BACKGROUND Atrial septal communications (ASCs) include atrial septal defects (ASDs) and patent foramen ovale (PFO). AIM The purpose of this study was to assess P-wave dispersion (PWD) and the prevalence of arrhythmia in patients before and after ASC closure. METHODS We analysed the clinical history and performed 12-lead electrocardiograms, echocardiograms, and 24-h Holter electrocardiograms in patients with ASC, before and six months after ASC closure. RESULTS We included patients with ASD (n = 56) and PFO (n = 73). PWD before percutaneous ASC closure was predicted by right ventricular outflow tract (RVOT) proximal diameter, left atrial area, ASD, smoking, and paroxysmal dyspnoea, R2 = 0.67; p < 0.001. RVOT proximal diameter was an independent predictor of PWD, both in patients with ASD and PFO. Six months after successful closure of ASC, a reduction in PWD was observed in the whole group of patients as well as in patients with ASD and PFO considered separately. A decrease in PWD was associated with reduction of maximum P-wave duration. At the same time, in the whole group, we noticed a reduction in the number of supraventricular and ventricular extrasystolic beats and fewer atrial fibrillation (AF) episodes, p < 0.04 for all variables. Postprocedural AF episodes in patients with ASD were predicted by PWD of 80 ms. CONCLUSIONS Percutaneous closure of ASC is associated with a reduction of PWD and fewer arrhythmia episodes six months after the procedure. PWD predicts AF episodes after ASD closure.