Accessory mitral valve tissue (AMVT) is a rare congenital cardiac anomaly sometimes responsible for left ventricular outflow tract (LVOT) obstruction. It is diagnosed during both neonate-childhood and adult periods in patients usually symptomatic for dyspnoea, chest pain, palpitations, fatigue, or syncope. Nevertheless, AMVT is often an incidental finding. AMVT is most often associated with other cardiac and vascular congenital malformations, such as septal defects and transposition of the great arteries. Surgery is indicated only in cases of significant LVOT obstruction and in patients undergoing correction of other cardiac malformations or exploration of an intracardiac mass. Two-dimensional echocardiography, both transthoracic and transoesophageal, is considered the main imaging modality for AMVT diagnosis and patient follow-up. The recent introduction of three-dimensional echocardiography allows a more realistic characterization of this entity. We present three clinical cases in which AMVT was incidentally diagnosed during standard echocardiography and an updated review of the literature highlighting the usefulness of echocardiography for AMVT morphological and functional characterization as well as the most relevant clinical implications due to its discovery.
An independent association between grade I left ventricular diastolic dysfunction and increased arterial stiffness is demonstrated at the earliest stage of heart failure. Hence, assessment of vascular function, beyond cardiac function, should be included in a comprehensive clinical evaluation of these patients.
Obstructive events during sleep in patients with obstructive sleep apnoea (OSA) cause large alterations in blood pressure, and this may lead to changes in baroreflex function with implications for long-term blood pressure control. This study examined the daytime variations in the responses to carotid baroreceptor stimulation in OSA patients. We determined the cardiac and vascular responses every 3 h between 09.00 and 21.00 h in 20 patients with OSA, using graded suctions and pressures applied to a neck collar. These responses were plotted against estimated carotid sinus pressures and, from these plots, baroreflex sensitivities and operating points were taken as the maximal slopes and the corresponding carotid sinus pressures, respectively. We found that at 09.00 h, sensitivity for the control of vascular resistance was at its lowest (−1.2 ± 0.2% mmHg −1 , compared with −1.9 ± 0.3% mmHg −1 at 12.00 h, P < 0.02) and operating point for control of mean arterial pressure was at its highest (101.1 ± 5.8 mmHg, compared with 94.1 ± 5.8 mmHg at 12.00 h, P < 0.05). This is in contrast to previous data from normal subjects, in whom sensitivity was highest and operating point lowest at 09.00 h. We suggest that the higher baroreflex sensitivity and lower operating point seen in the mornings in normal subjects may provide a protective mechanism against hypertension and that this protection is absent in patients with OSA. It is possible that the reduced reflex sensitivity and increased operating point in the mornings may actually promote hypertension.
1. Although leptin increases sympathetic nerve activity and blood pressure, its direct action on large arterial rings is to cause relaxation. However, it is the small resistance arteries and veins that are important in blood pressure control. The effects of leptin on these small vessels has not been reported previously in the canine and the effect of leptin on the capacitance vessels is not known. 2. In the present study, third- or fourth-order canine mesenteric arteries and veins were isolated and placed in a perfusion myograph and preconstricted with noradrenaline. The responses to graded concentrations of leptin were determined and the role of nitric oxide was assessed by administration of N(G)-nitro-l-arginine methyl ester (l-NAME), a blocker of nitric oxide synthase. 3. Leptin induced dose-related dilatations in both arterial and venous segments. The mean (+/-SEM) maximum increases in the diameter of the arteries and veins were 25.0 +/- 4.8 and 29.9 +/- 2.0% of the initial preconstriction, respectively. Relaxations of both arteries and veins were abolished by l-NAME or by endothelium denudation, although dilatations were still obtained to sodium nitroprusside, a nitric oxide donor. 4. These results indicate that leptin dilates canine small mesenteric arteries and veins by a mechanism involving endothelial release of nitric oxide. This observation may result in a decrease of peripheral resistance and venous return and, hence, counteract the leptin-induced neurally mediated vasoconstriction that has been reported previously.
In a population with normal carotid IMT and without plaques, changes in arterial stiffness are significantly related to the number of risk factors. This information could be relevant for a more tailored primary prevention in patients with risk factors even in absence of structural atherosclerotic abnormalities.
In Echo-Lab, Rome, Italy, the integrated cardiovascular ultrasound study is feasible in a high percentage of patients. The combination of three parameters, that is, score of calcium, cIMT, and LAD velocity, has incremental predictive value for obstructive CAD.
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