Pasquale Crea

Takotsubo syndrome and estrogen receptor genes: partners in crime?

Aims We aimed to analyze genetic polymorphism of estrogen receptor (ESR) 1 and ESR2 in a series of postmenopausal women with Takotsubo syndrome (TS). Methods In total, 81 consecutive white women were prospectively enrolled: 22 with TS (TS group; mean age 71.2 ± 9.8 years), 22 with acute myocardial infarction (MI group; mean age 73.2 ± 8 years), and 37 asymptomatic healthy controls (CTRL group; mean age 69 ± 4.2 years). Genotyping of ESR1 −397C>T (rs2234693) and −351A>G (rs9340799) and ESR2 −1839G>T (rs 1271572) and 1082G>A (rs1256049) genetic variants was performed. We estimated the odds ratio (OR) between the genotype of each examined locus with the occurrence of TS or MI. Results The risk of experiencing TS was higher for those study participants carrying the T allele at the rs2234693 locus of the ESR1 gene [OR: 2.0, 95% confidence interval (CI): 0.973–4.11, P = 0.04, TS vs. MI + CTRL; OR: 2.79, 95% CI: 1.17–6.64, P = 0.016, TS vs. MI alone]. Women carrying a T allele at the rs1271572 locus of the ESR2 gene demonstrated an even higher risk (OR: 3.23, 95% CI: 1.55–6.73, P = 0.0019, TS vs. MI + CTRL; OR: 9.13, 95% CI: 2.78–29.9, P = 0.0001, TS vs. MI alone). Conclusion The study reports preliminary findings suggesting a possible link between ESR polymorphisms and the occurrence of TS. Larger studies are needed to confirm our results.

SafeR and escape junctional rhythm: A singular trigger for pacemaker-mediated tachycardia

A 70-year-old man, who previously received a dual chamber pacemaker for paroxysmal AV block (Sorin Symphony DR 2550), was noted on telemetry to have multiple episodes of rapid ventricular pacing at approximately 120bpm. Evaluation of the telemetry strips revealed that all of the rapid ventricular pacing episodes were initiated by brief runs of escape junctional rhythm. Programmed bradycardia parameters were AAI SafeR with lower rate limit of 50bpm.

Image Diagnosis: Pericardial Cyst in a Dialysis Patient

Pericardial cysts are rare, usually benign congenital anomalies but may also be acquired. They represent 6% of mediastinal masses and 33% of all mediastinal cysts.1) The vast majority are asymptomatic and are usually found incidentally on chest radiographs, computed tomography scans, magnetic resonance images, or echocardiography.2) Large pericardial cysts may cause compression on adjacent structures and organs, resulting in dyspnea, chest pain, or persistent cough.3) There have been reports of cyst rupture, cardiac compression, atrial fibrillation, and even sudden cardiac death from these cysts, although these complications are uncommon.4) A 55-year-old Italian dialysis patient with a shortness of breath, asthenia and excessive fatigability was referred to our institution. He had history of pericarditis, myocarditis and massive pleural effusion. His electrocardiogram showed sinus rhytm. Transthoracic echocardiography (TTE) revealed normal left and right ventricular systolic performance, with normal wall thicknesses and chamber sizes and a pericardial thickening. Color Doppler imaging showed a mild mitral and tricuspid regurgitation. Apical and subcostal views of TTE showed an oval echolucent structure at the right cardiophrenic angle, minimally compressing the right atrium, and of approximately 10 × 4 cm, consistent with a pericardial cyst (Fig. 1). Cardiac magnetic resonance (CMR) confirmed echocardiography findings, showing the presence of the pericardial cyst with several fibrinous strands inside associated with right-sided massive pleural effusion. Late gadolinium-enhanced CMR images showed intramural myocardial enhancement in anterior and inferior wall and enhancement of pericardium, as an expression of myocardial and pericardial inflammation (Fig. 2). The patient was treated conservatively because of high surgical risk attributed to severe kidney failure. A repeated TTE with the apical 4-chamber view at 20 months later showed minimal increase in the size of the pericardial cyst. The discovery of a pericardial cyst obliges the clinician to perform a broad differential diagnosis with a coronary artery aneurysm, dextrocardia, malignancy, and even pneumonia.5) CMR may help in this diagnosis. Fig. 1 Echocardiographic evaluation revealed a pericardial cyst in the inferior wall of the left ventricle. Fig. 2 Vertical long-axis (A and D) and short-axis (B, C, E, and F) cardiac magnetic resonance (CMR) images of pericardial cyst in patient with pericarditis, myocarditis and massive pleural effusion. Cyst (white asterisks) has low signal intensity on T1-weighted ...

Resynchronization therapy in heart failure with right bundle branch block: new perspectives

To the Editor: We enjoyed reading the interesting article by Giudici et al. [1], recently published in this Journal, about the effects of right ventricular (RV) septal pacing in patients with right bundle branch block (RBBB). Synchronized RV septal pacing was found to significantly reduce QRS duration with almost normalization of the ECG. Cardiac resynchronization therapy (CRT) by biventricular pacing is recommended, in addition to optimal medical therapy, in selected patients with congestive heart failure (CHF), advanced left ventricular (LV) systolic dysfunction and prolonged QRS interval. Objective of biventricular pacing is to restore atrio-ventricular (A-V), inter-ventricular (V-V) and intra-LV synchrony in order to reduce symptoms and to improve cardiac function and outcomes. The presence of a typical left bundle branch block (LBBB) morphology of the QRS complex is a strong predictor of response to CRT with biventricular pacing, whereas right bundle branch block (RBBB) morphology and non-specific intra-ventricular conduction disturbances are associated with a low rate of response. This holds true especially in patients with isolated RBBB (namely, in absence of left anterior or posterior hemiblock). In this condition, the left bundle branch is preserved and, probably, LV pacing is unnecessary if not self-defeating. As reported in this study [1], a septal positioning of the RV lead, joined to an opportune A-V setting, could turn a dual chamber device into a de facto CRT device. This occurs thanks to an optimal fusion between right ventricular septal stimulation and preserved left bundle branch conduction, leading to a significant narrowing of QRS complex. The results of this initial pilot study are encouraging, as they suggest that this pacing technique in patients with RBBB is feasible and safe. The study, however, did not specifically evaluate patients with CHF, as the population included both patients receiving pacemaker for conventional indications to cardiac pacing and patients receiving implantable cardioverter defibrillator (ICD) for primary or secondary prevention [1]. Some months ago we had reported in this Journal a case of normalization of QRS duration after RV septal pacing in a patient with refractory CHF and RBBB receiving ICD for primary prevention [2]. Also in our case, a significant narrowing of QRS complex (from 180 ms to 100 ms) had been obtained with a dual chamber device, thanks to a fusion

Negative concordant T waves during paced ventricular rhythm: An honest enemy is better than a false friend

The ECG diagnosis of myocardial infarction and ischemia in pacemaker patients is often challenging. The three criteria, proposed by Sgarbossa et al. in 1996, useful to suspect myocardial ischaemia in patient with left bundle branch block were demonstrated to be valid also in pacemaker patients. In the last years, concordant negative T waves in patients with ventricular paced rhythm were linked to various expressions of acute myocardial injury. If available, comparison with previous ECG is crucial. Partial persistence of cardiac memory during fusion beats created an anomalous concordance between negative T waves and QRS axis and could induce erroneous suspicions. AV delay modification could help to unmask this situation.

Spike on T wave! What went wrong?

An 80-year-old male, who previously received a dual chamber pacemaker, was referred to our ambulatory for dizziness and fatigue. The ECG obtained showed sinus rhythm, highly variable atrioventricular (AV) interval and alternation between spontaneous and paced ventricular complexes. A spike on the ascending part of the T wave was observed, suggesting ventricular undersensing. However, telemetry-supported pacemaker control showed inconstant atrial undersensing.

Functional atrial undersensing associated with device algorithm promoting AV conduction

A 58-year-old woman received a dual chamber pacemaker (Medtronic) for sick sinus syndrome. Given intact AV conduction the Managed Ventricular Pacing mode algorithm (MVP) was programmed. The day after, she suffered from palpitations. Her ECG showed a possible loss of atrial capture accompanied by atrial undersensing. Telemetry-supported pacemaker control confirmed the loss of capture. Undersensing of atrial signal was functional, related to long atrial refractory period in MVP mode algorithm. Device algorithms could induce false suspicions. Awareness about the different pacing algorithms can be useful in order to avoid erroneous interpretations and to correct potential malfunctioning.

V > A: When the paradigm fails!

AFilipino45-year-oldmanwith a history of coronary heart disease and congestive heart failure (CHF), who previously received a biventricular cardioverter defibrillator (Quadra AssuraMP 3371-40C St. JudeMedical, Abbott, St. Paul, MN, USA), was admitted for palpitations. He was receiving optimalmedical therapy for CHF (namely loop diuretic, betablocker, angiotensin-converting-enzyme [ACE]-inhibitor, aldosterone antagonist, and ivabradine) besides aspirin. The electrocardiogram (ECG) showed wide QRS tachycardia at 160 beats per minute (bpm) with a singular bigeminal rhythm (see Fig. 1). The patient was hemodynamically stable (arterial bloodpressure [ABP] 130/80mmHg). ContinuousECGmonitoringandaperipheral venousaccesswereobtained. QRS complexes had a typical right bundle branch block with left anterior hemiblock morphology, suggesting supraventricular tachycardia (SVT) with aberrancy. Analysis of lead V1 (where P wave was better observable) was not conclusive for atrial flutter/atrial tachycardia diagnosis or atrio-ventricular (AV) dissociation. A clear P wave was seen after the second QRS complex of any couple. Other atrial activity waves could have been partially hidden by wide QRS complexes. Previous ECGs were not immediately available. Telemetry-supported pacemaker control was performed in order to facilitate a diagnosis. It showed 3 arrhythmic episodes in VT2 zone, each one interrupted after single burst of antitachycardia pacing therapy (ATP; see Fig. 2). Surprisingly, ventricular rate was double than atrial activity, suggesting ventricular tachycardia (VT) diagnosis. Current EGMs were identical. What is themechanism of this bigeminal tachycardia?

A Case of Brugada Pattern Migrant from Right Precordial Leads to Peripheral Leads

Since the first report in 1992, Brugada pattern (BP) diagnosis is mainly based on analysis of the precordial leads. In cases with no clear BP evidence in the conventional right precordial leads (4th intercostal space), limb leads analysis resulted helpful in suspecting BP. Fluctuations within right precordial leads between the diagnostic ECG pattern and nondiagnostic ECGs are well known. For the first time, in the patient herewith reported, the transformation of BP phenotype involves both precordial and peripheral leads, confirming that the analysis of all the 12 leads has a key role in BP diagnosis.

The Role of Echocardiography in the Evaluation of Cardiac Damage in Hypertensive Obese Patient

Obesity rates are rising worldwide. Often obesity is associated with hypertension leading to an increased cardiovascular risk. Both obesity and hypertension induce several modifications in cardiac structure and function, particularly atrial and ventricular remodeling is a common finding shared by these two conditions. It has been demonstrated obesity leads to: left ventricular (LV) mass increase, LV systolic and diastolic dysfunction, left atrium (LA) size increase, LA function alterations and pericardial fat accumulation. Nowadays, the development of cardiac imaging techniques allows to early identifying any preclinical damage related to hypertension and obesity. This could be very important in order to improve patient management and medical therapy.