Ultrasound-guided Axillary Vein Puncture for Cardiac Device Implantation: A Safe and Effective Approach.

Ultrasound-guided axillary vein access is an effective alternative to conventional subclavian and cephalic access for cardiac implantable electronic device implantation. The aim of this study was to compare the safety, efficacy, and radiation exposure data of the ultrasound-guided axillary approach with other conventional access techniques. The study population included 130 consecutive patients, stratified as 65 (64% male; median age, 79 years) in the study group and 65 (66% male; median age, 81 years) in the control group. We performed a retrospective not-randomized analysis by comparing ultrasound-guided axillary vein puncture with subclavian and cephalic approaches in order to test the effect on X-ray exposure, total procedure time, and complications. Significant differences were observed in terms of radiation exposure, including fluoroscopy time (median, 95 s [study group] vs. 193 s [control group]; P < .001), air kerma (median, 29 mGy [study group] vs. 55.7 mGy [control group]; P < .001), and dose-area product (median, 8219 mGy·cm2 [study group] vs. 16736 mGy·cm2 [control group]; P < .001). The median procedure time was 45 min in the study group but 50 min in the control group (P < .05). Complications occurred in 6 control group patients (1 urticaria contrast medium-related, 3 pneumothorax, 2 subclavian artery puncture) and 2 study group patients (2 axillary artery puncture). We conclude that the ultrasound-guided axillary venous approach is a fast, feasible, and safe technique for cardiac lead implantation. It allows a significant reduction in fluoroscopy time without prolonging the procedural time. This approach offers direct visualization of the vessel during the puncture, so it can be useful in patients who cannot receive contrast medium, those who require "difficult" thoracic approaches (emphysema, too much or too little fat tissue), or those on anticoagulant therapy.

Takotsubo syndrome and pheochromocytoma: an insidious combination.

Pheochromocytoma is a rare adrenal tumor characterized by the secretion of catecholamines and vasoactive peptides. It can cause a catecholaminergic storm and lead to acute coronary syndromes. We present the case of a 53-year-old man, without any medical history, who arrived to the hospital following a spinal trauma due a fall. He presents back and retrosternal pain, with a clinical status of acute pulmonary edema, sinus tachycardia with left bundle branch block, left ventricular apical ballooning with depressed systolic function. Blood tests show a very important increase of Troponin and transaminases. A contrast chest-abdomen CT highlighted a right adrenal solid mass, with a diameter of 78mm, partial capsular laceration, compression of the inferior vena cava and the hepatic parenchyma. The clinical condition of the patient rapidly worsens from a respiratory and hemodynamic point of view, with cardiogenic shock, anuria and sepsis, refractory to all the medical treatments, until the patient died. The autopsy confirmed that the abdominal mass was a pheochromocytoma, broken after the trauma suffered. The resulting catecholaminergic storm caused a myocardial ischemia with Takotsubo syndrome, with cardiogenic shock. This unfortunate case confirms the pheochromocytoma as important risk factor for the onset of Takotsubo syndrome, and the how dramatic and severe a catecholaminergic storm can be.

Myocardial scar location as detected by cardiac magnetic resonance is associated with the outcome in heart failure patients undergoing surgical ventricular reconstruction.

OBJECTIVES: Post-infarction myocardial scar causes adverse left ventricular remodelling and negatively affects the prognosis. We sought to investigate whether scar extent and location obtained by cardiac magnetic resonance may affect the reverse remodelling and survival of heart failure patients undergoing surgical ventricular reconstruction. METHODS: From January 2011 to December 2015, 151 consecutive patients with previous myocardial infarction and left ventricular remodelling underwent surgical ventricular reconstruction at our Institution, of which 88 (58%) patients had a preoperative protocol-standardized late gadolinium enhancement (LGE)-cardiac magnetic resonance examination during the week before surgery. We excluded 40 patients with devices (26%), 15 patients with irregular heart rhythm (permanent atrial fibrillation, 10% not included in the device group) or mixed contraindications (severe claustrophobia or presence of material magnetic resonance not compatible). Among the 145 survivors, 11 patients received an implantable cardioverter defibrillator after surgery (mostly for persistent low ejection fraction) and were excluded as well, yielding a total of 59 patients (48 men, aged 65 ± 9 years) who repeated a protocol-standardized LGE-cardiac magnetic resonance examination even 6 months postoperatively and therefore represent the study population. Patients were grouped according to the presence of LGE in the antero-basal left ventricular segments (Group A) or the absence of LGE in the same segments (Group B). The postoperative left ventricular end-systolic volume index was considered the primary end-point. RESULTS: After surgery, left ventricular end-systolic volume index and end-diastolic volume index significantly decreased (P < 0.001, for both), while diastolic sphericity index and ejection fraction significantly increased (P = 0.015 and P < 0.001, respectively). The presence of LGE in the antero-basal left ventricular segments (10 patients, Group A) was the only independent predictor of outcome (P = 0.02) at multivariate analysis, being the postoperative left ventricular end-systolic volume index significantly higher compared to that of patients of Group B (49 patients) (78 ± 26 ml/m2 vs 55 ± 20 ml/m2, P = 0.003). Furthermore, patients with a postoperative left ventricular end-systolic volume index >60 ml/m2 showed a higher risk of cardiac events (hazard ratio = 3.67, P = 0.02). CONCLUSIONS: In patients undergoing surgical ventricular reconstruction, LGE scar location affects the left ventricular reverse remodelling, which in turn might limit the survival benefit.

Evidence of increased platelet reactivity in the first six months after acute ST segment elevation myocardial infarction.

INTRODUCTION: Platelets play a crucial role in the pathogenesis of acute coronary syndromes. Accordingly, previous studies showed increased platelet reactivity on admission in these patients. In this study we assessed platelet reactivity at short-medium term follow-up in patients with ST-segment elevation acute myocardial infarction (STEMI). MATERIALS AND METHODS: Fifty-nine patients (58 ± 11 years, 45 men), treated with primary angioplasty, were studied 1 month after STEMI. Thirty-five patients were retested at 6 months. Twenty matched patients with stable coronary artery disease served as controls. Platelet reactivity was assessed by flow cyometry at rest and at peak exercise, with and without adenosine diphosphate (ADP) stimulation, by measuring monocyte-platelet aggregates (MPAs) and glycoprotein IIb/IIIa (CD41) expression in the MPA gate, and CD41 and fibrinogen receptor (PAC-1) expression in the platelet gate. RESULTS: Compared to controls, basal MPAs and CD41 in the MPA gate were higher in STEMI patients both at 1 month (p = 0.001 and p = 0.002, respectively) and at 6 months (p = 0.03 and p = 0.01, respectively). Basal CD41 and PAC-1 expression was also higher in STEMI patients at the two assessments compared to controls (P<0.001 for both). Exercise induced a similar increase in platelet reactivity in patients and controls. ADP induced a higher increase in CD41 platelet expression in STEMI patients compared to controls both at 1 and 6 months (P < 0.001). CONCLUSION: Platelet reactivity is increased in the first 6 months after STEMI. The persistence of increased platelet reactivity in this time period may play a role in the early recurrence of coronary events after STEMI.

Relation between cardiovascular risk factors and coronary microvascular dysfunction in cardiac syndrome X.

BACKGROUND: The causes of coronary microvascular dysfunction (CMVD) in patients with cardiac syndrome X (CSX) are largely unknown. Common cardiovascular risk factors (CVRFs) and increased markers of inflammation have been associated with CMVD in some studies, but their role in determining CMVD in CSX patients remains poorly known. METHODS AND RESULTS: We studied 71 CSX patients (56 ± 9 years, 23 men) and 20 healthy volunteers (52 ± 7 years, nine men). Using transthoracic Doppler echocardiography, coronary microvascular vasodilator function was assessed in the left anterior descending coronary artery as the ratio of diastolic coronary blood flow (CBF) velocity at peak intravenous adenosine administration and during cold pressor test (CPT) to the respective basal CBF velocity values. Common CVRFs tended to be more frequent and C-reactive protein (CRP) levels were higher (P < 0.001) in CSX patients than in controls. Both CBF responses to adenosine (2.05 ± 0.6 vs. 2.92 ± 0.9, P < 0.001) and to CPT (1.71 ± 0.6 vs. 2.42 ± 0.7, P < 0.001) were lower in CSX patients than in controls. The differences between the two groups in CBF response to adenosine and in CBF response to CPT remained highly significant (P < 0.01 for both) after adjustment for all CVRFs, including serum CRP levels. CONCLUSION: In CSX patients, both endothelium-dependent and endothelium-independent CMVD cannot be reliably predicted by CVRFs (including serum CRP levels), alone or in combination.