Numerical validation of a new method to assess aortic pulse wave velocity from a single recording of a brachial artery waveform with an occluding cuff

Recently a new method has been proposed as a tool to measure arterial pulse wave velocity (PWV), a measure of the stiffness of the large arteries and an emerging parameter used as indicator of clinical cardiovascular risk. The method is based on measurement of brachial blood pressure during supra-systolic pressure inflation of a simple brachial cuff (the device is known as the Arteriograph (Tensiomed, Budapest, Hungary)). This occlusion yields pronounced first and secondary peaks in the pressure waveform, the latter ascribed to a reflection from the aortic bifurcation, and PWV is calculated as the ratio of twice the jugulum-symphysis distance and the time difference between the two peaks. To test the validity of this working principle we used a numerical model of the arterial tree to simulate pressures and flows in the normal configuration, and in a configuration with an occluded brachial artery. A pronounced secondary peak was indeed found in the brachial pressure signal of the occluded model, but its timing was only related to brachial stiffness and not to aortic stiffness. We also compared PWV’s calculated with 3 different methods: PWVATG (~ Arteriograph principle), PWVcar-fem (~ carotid-femoral PWV, the current clinical gold standard method) and PWVtheor (~ Bramwell-Hill equation). Both PWVATG (R²=0.94) and PWVcar-fem (R²=0.95) correlated well with PWVtheor, but their numerical values were lower (by 2.17 ± 0.42 and 1.08 ± 0.70 m/s for PWVATG and PWVcar-fem, respectively). In conclusion, our simulations question the working principle of the Arteriograph. Our data indicate that the method picks up wave reflection phenomena confined to the brachial artery, and derived values of PWV rather reflect the stiffness of the brachial arteries

Late cardiotoxicity after low dose of anthracycline therapy for acute lymphoblastic leukemia in childhood

Introduction Late cardiotoxicity is a known complication of anthracycline therapy but the long-term effects of low cumulative doses are not well documented. We studied late cardiotoxicity in survivors of childhood acute lymphoblastic leukemia (ALL) treated with low anthracycline doses 10 to 20 years earlier. Methods Seventy-seven ALL survivors who received a cumulative anthracycline dose <250 mg/m(2) and were at least 10 years after treatment were evaluated for signs of clinical heart failure. Cardiac function was assessed by echocardiography including tissue Doppler measurements of the septal mitral annulus in 37 ALL survivors 10.6-18.3 years (median 13.3 years) after anthracycline treatment with cumulative doses of 180 (n=19) or 240 mg/m(2) (n=18). The control group consisted of 30 healthy volunteers matched for age, sex, BSA, and BMI. Results No clinical relevant cardiotoxicity was found. Left ventricular shortening fraction (SF) was significantly reduced in male ALL survivors. Three of the 19 male ALL survivors had an SF below 30%. Male ALL survivors showed a significantly lower early filling velocity to atrial contraction velocity ratio but myocardial velocity during early filling was comparable between patients and controls. ALL survivors had a significantly longer isovolumetric relaxation time (IVRT). Thirty percent of the ALL survivors have an abnormal IVRT compared to the normal range of the controls. Conclusion and implications for cancer survivors At a median of 13.3 years after exposure to cumulative doses of anthracyclines of 180 or 240 mg/m(2), no clinical relevant cardiotoxicity was found but subclinical cardiac abnormalities were present in 30% of the patients

Closure of a lateral baffle leak in a Fontan patient with an Amplatzer PDA II AS plug

Cyanosis after Fontan surgery or surgery for total cavopulmonary connection (TCPC), due to different types of communications (fenestration, venovenous collaterals or fistula), is not uncommon. We present the case of an 8-year-old girl presenting with increasing cyanosis during exercise 4 years after an intracardiac TCPC with lateral tunnel. Angiography showed a fistulous trajectory originating at the superior vena cava towards the base of the right atrial appendage. Due to the difficult anatomy in our patient, closure with conventional devices was not possible. We finally used a new Amplatzer PDA II AS plug to successfully close the fistula. In conclusion, closure of lateral baffle leak and device choice in case of difficult anatomy can be cumbersome. The new PDA II AS type plug can offer an elegant alternative for successful closure of some fistula

Spontaneous aortic arch thrombosis in a neonate

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Transthoracic echocardiography guidance of transcatheter atrial septal defect closure in children

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Unsuccessful resuscitation of a preterm infant due to a pneumothorax and a masked tension pneumopericardium

Pneumopericardium is the least common form of air leak in infants. A tension pneumopericardium is even more infrequent but associated with a very high mortality rate. We describe the case of an unsuccessful resuscitation in a preterm infant due to a pneumothorax and tension pneumopericardium. Despite relatively mild pressure ventilation the patient developed massive pulmonary interstitial emphysema. The extra-alveolar air spread from the interstitium towards the mediastinal space (Macklin effect) and caused a pneumothorax and pneumopericardium, which evolved towards a tension pneumopericardium after a traumatic mechanical procedure. The infant deteriorated acutely. Despite prompt pleural drainage there were no signs of recovery at any time. Postmortal examination revealed a tension pneumopericardium and massive interstitial pulmonary emphysema, which was not obvious on radiographical investigation. In cases of acute deterioration of a ventilated neonate, one should always rule out pneumothorax. If the patient does not recover after pleural drainage and cardiac resuscitation a (tension) pneumopericardium should be considered.status: publishe