Cardiac Arrhythmias and Acute Cerebrovascular Events: A Case of QT Prolongation and Torsades de Pointes Early After Right Insular Stroke.

Stroke involving some areas of the cerebral hemisphere, such as insula, amygdala, and lateral hypothalamus, may cause changes in autonomic control of cardiac function. A 58-year-old woman presented to the emergency department for acute onset of left facial-brachial-crural hemiparesis and dysarthria. A brain CT scan showed subacute ischemic lesion with hemorrhagic infarction in right insular-rolandic cortex. Over the next few days ECG showed severe bradycardia with elongation of QTc, significative pauses (5 seconds), runs of nonsustained ventricular tachycardia and torsades de pointes. Drug induced and other several possible causes of elongation of QT and bradycardia such as hypokalemia, a history of heart failure, and structural heart disease were ruled out. The case confirms that insular cortex plays a major role in stroke-induced cardiovascular changes.

[Paclitaxel-coated balloons for in-stent restenosis treatment: long-term clinical results and predictors of recurrent target lesion revascularization]. / Palloncini medicati a eluizione di paclitaxel nel trattamento delle ristenosi intrastent: risultati clinici a lungo termine e predittori di nuova rivascolarizzazione della lesione bersaglio.

BACKGROUND: The aim of this study was to report clinical outcomes in patients treated with paclitaxel-coated balloons (PCB) for in-stent restenosis (ISR) in both bare metal (BMS) and drug-eluting stent (DES). METHODS: Between May 2009 and December 2015, we treated 155 ISR in 140 patients. At recruitment, 35% of patients had diabetes. Among the lesions, 125 were first occurrence (55 within BMS and 70 within DES) and 30 recurrent; 24 ISR were multi-metal layered. Mean reference diameter was 2.79 ± 0.52 mm and mean lesion length 13.2 ± 7.1 mm. PCB use included 32 Dior I, 97 InPact Falcon, 18 Panthera Lux, and 8 Restore DEB. RESULTS: At a median follow-up of 442 days, we observed 18 target lesion revascularizations (TLR), one myocardial infarction, 3 cardiac deaths, and 5 non-cardiac deaths. TLR occurrence differed according to type of ISR (4% within BMS, 14% within DES, 28% within recurrent ISR; p<0.05). TLR was associated with PCB type (35% Dior I, 9% InPact Falcon, 0% Panthera Lux and Restore DEB; p<0.05). Multivariable analysis revealed that first-generation PCB without a carrier (hazard ratio [HR] 2.50, 95% confidence interval [CI] 0.96-6.50; p=0.06) and recurrent ISR (HR 7.76, 95% CI 1.56-38.66; p=0.01) correlated with subsequent TLR. CONCLUSIONS: Our results confirm the safety and efficacy of PCB for ISR treatment both within BMS and DES. PCB type and recurrent ISR correlate with subsequent TLR.

The missing link between atherosclerosis, inflammation and thrombosis: is it tissue factor?

Acute thrombus formation on disrupted atherosclerotic plaques plays a key role during the onset of acute coronary syndromes. Lesion disruption facilitates the interaction between circulating blood and prothrombotic substances, such as tissue factor (TF) present within the atherosclerotic lesion. For a long period of time, vessel-wall TF has been considered the major determinant of thrombosis. However, this old dogma has been recently changed owing to the discovery of a different pool of TF that circulates in flowing blood (blood-borne TF). Several studies have shown that blood-borne TF circulates in different pools that are associated with selected blood cells, such as monocytes, granulocytes and platelets in cell-derived microparticles, and as a soluble protein generated by alternative splicing of its full-length mRNA. Recent studies have identified a hypercoagulable state associated with an increased circulating TF activity, leading to the concept of 'vulnerable blood'. Part of the blood-borne TF circulates in an 'inactive' form and it is required to be 'activated' to exert its thrombogenic potential. Certain pathological conditions, such as smoking, hyperlipidemia and diabetes, show a higher incidence of thrombotic complications. These conditions are also characterized by the presence of high levels of circulating TF activity. Recent evidence may also suggest that an increased circulating TF activity may potentiate the initial thrombogenic stimulus represented by vessel wall-associated TF, leading to the formation of larger and/or more stable thrombus, and thus more severe acute coronary syndromes. It has been reported that inflammation increases TF expression and activity by different cell types. On the other hand, TF upregulation may facilitate inflammation by enhancing intravascular fibrin deposition, formation of proinflammatory fragments of fibrin, and by generating coagulation proteases, including FVIIa, FXa and thrombin, that activate protease-activated receptors. Furthermore, the biology of TF is know known to be more complex than previously thought by the demonstration that this protein, apart from its known effects on blood coagulation, can also function as a signaling receptor.