Erik Andries’s research while affiliated with OLV Ziekenhuis Aalst and other places

Although most malignant tumours metastasize to the heart they rarely produce clinical symptoms. Cardiac metastasis of tumours arising from head and neck and particulary of the larynx are extremely rare. Herein we report an unusual case of successfully treated, advanced laryngeal carcinoma with subsequent late symptomatic metastatic disease to the heart. The patient discussed, developed a right ventricular intracavitary tumour with pseudo-infarct pattern on the ECG. Current litterature regarding incidence, diagnostic techniques, treatment modalities and survival rates of secondary heart tumours are reviewed.

Although most malignant tumours metastasize to the heart they rarely produce clinical symptoms. Cardiac metastasis of tumours arising from head and neck and particulary of the larynx are extremely rare. Herein we report an unusual case of successfully treated, advanced laryngeal carcinoma with subsequent late symptomatic metastatic disease to the heart. The patient discussed, developed a right ventricular intracavitary tumour with pseudo-infarct pattern on the ECG. Current litterature regarding incidence, diagnostic techniques, treatment modalities and survival rates of secondary heart tumours are reviewed.

The oxygen uptake efficiency slope (OUES) is a new submaximal parameter which objectively predicts the maximal exercise capacity in children and healthy subjects. However, the usefulness of OUES in adult patients with and without advanced heart failure remains undetermined. The present study investigates the stability and the usefulness of OUES in adult cardiac patients with and without heart failure. Forty-five patients with advanced heart failure (group A) and 35 patients with ischemic heart disease but normal left ventricular ejection fraction (group B) performed a maximal exercise test. PeakVO2 and percentage of predicted peakVO2 were markers of maximal exercise capacity, whereas OUES, ventilatory anaerobic threshold (VAT), and slope VE/VCO2 were calculated as parameters of submaximal exercise. Group A patients had lower peakVO2 (P < .001), lower percentage of predicted peakVO2 (P = .001), lower VAT (P < .05), steeper slope VE/VCO2 (P < .001), and lower OUES (P < .02). Within group A, significant differences were found for VAT, slope VE/VCO2, and OUES (all P < .01) between patients with peakVO2 above and below 14 mL O2/kg/min. Of all the submaximal parameters, VAT correlated best with peakVO2 (r =.814, P < .01) followed by OUES/kg (r = .781, P < .01), and slope VE/VCO2 (r = -.492, P < .001). However, VAT could not be determined in 18 (23%) patients. OUES remains stable over the entire exercise duration and is significantly correlated with peakVO2 in adult cardiac patients with and without impaired LVEF. Therefore, OUES could be helpful to assess exercise performance in advanced heart failure patients unable to perform a maximal exercise test. Further studies are needed to confirm our hypothesis.

We describe a patient with hemodynamic deterioration and worsening mitral regurgitation related to right ventricular apex pacing. Time-dependent changes in papillary muscle contraction as well as ventricular remodeling by right ventricular apex pacing might be responsible for this rare but serious complication.

Neurocardiogenic dysfunction is believed to result from activation of ventricular mechanoreceptors. To asses other humoral and circulatory mechanisms activated during vasovagal syncope, epinephrine, norepinephrine, renin, and aldosterone levels were measured during head-up tilt testing. Twenty-three patients referred because of vasovagal syncope underwent passive head-up tilt testing (80 degrees). Blood samples were taken at baseline, after 30 minutes of supine rest and at syncope. Five patients (four men, one woman; mean age 46 +/- 27 years) had cardioinhibitory syncope. Seven patients (five men, two women; mean age 40 +/- 12 years) had vasodepressor syncope. Eleven patients (eight men, three women; mean age 55 +/- 21 years) had negative results of head-up tilt tests. Among patients with cardioinhibitory syncope, norepinephrine concentration rose significantly from baseline to syncope (0.44 +/- 0.12 ng/ml versus 1.14 +/- 0.72 ng/ml; p < 0.05), whereas no significant change was observed in epinephrine (0.08 +/- 0.03 ng/ml versus 2.74 +/- 2.85 ng/ml; p = not significant [NS]), renin (5.68 +/- 3.03 pg/ml versus 19.58 +/- 11.47 pg/ml; p = NS), or aldosterone concentration (66.60 +/- 16.10 ng/ml versus 109.00 +/- 44.70 ng/ml; p = NS). Patients with vasodepressor syncope had a significant rise in renin (9.03 +/- 4.56 pg/ml versus 52.53 +/- 41.63 pg/ml; p < 0.05) and aldosterone concentration (95.43 +/- 103.03 ng/ml versus 249.57 +/- 191.54 ng/ml; p < 0.05), whereas no change in level of epinephrine (0.12 +/- 0.12 ng/ml versus 0.28 +/- 0.33 ng/ml; p = NS) or norepinephrine (0.60 +/- 0.26 ng/ml versus 0.86 +/- 0.53 ng/ml; p = NS) was detected. Among patients with negative results of tilt tests, levels of renin (7.94 +/- 7.19 pg/ml versus 27.71 +/- 18.50 pg/ml; p < 0.01) and aldosterone (64.64 +/- 28.33 ng/ml versus 160.91 +/- 79.58 ng/ml; p < 0.01) rose significantly, whereas no change was seen in epinephrine (0.12 +/- 0.14 ng/ml versus 0.23 +/- 0.31; p = NS) or norepinephrine concentration (0.54 +/- 0.21 ng/ml versus 0.82 +/- 0.52; p = NS). Patients with cardioinhibitory syncope were characterized by a rise in norepinephrine level and blunted activation of the renin-angiotensin-aldosterone axis at syncope. Unlike patients with cardioinhibitory syncope, the renin-angiotensin-aldosterone axis is activated in patients with vasodepressor syncope and patients with a negative result of head-up tilt test without a statistically significant increase in catecholamine levels. Patients with cardioinhibitory syncope have higher epinephrine levels at syncope compared with patients with a negative result of head-up tilt test and patients with vasodepressor syncope.

Radiofrequency ablation of the atrioventricular conduction system (ACS) has become an established therapy for patients with drug refractory atrial fibrillation. We observed eight patients with hemodynamic deterioration after radiofrequency ablation of the atrioventricular conduction system. As we found hemodynamic deterioration related to worsening mitral regurgitation, we compared the clinical history, electrophysiological, and echocardiographic data from the patients with hemodynamic deterioration and worsening mitral regurgitation (group 1) to those without hemodynamic deterioration and stable mitral regurgitation after the procedure (group 2). Eight out of 108 patients (7.4%) undergoing ablation of the ACS deteriorated hemodynamically with acute pulmonary edema in three and congestive heart failure in five patients occurring at a mean of 3 and 8 weeks, respectively, after the procedure. Three of these patients were referred for mitral valve surgery. Two patients underwent ablation using a left-sided approach. A right-sided approach was used in five patients. In one patient, a left- and right-sided approach was used. Compared to group 2 patients, group 1 patients had significantly higher left ventricular end-diastolic diameters (64 +/- 6 mm vs 56 +/- 9 mm) at baseline despite similar fractional shortening (32% +/- 11% vs 34% +/- 13%), left ventricular end-systolic diameters (43 +/- 9 mm vs 36 +/- 7 mm) and degree of mitral regurgitation (1.4 +/- 1.1 vs 1.4 +/- 0.7) on echocardiographic analysis. Thus, hemodynamic deterioration together with progression of mitral regurgitation is a potential complication of ablation of the ACS (up to 7.4%). Patients with high left ventricular end-diastolic diameters and moderate mitral regurgitation at baseline seem prone to this complication.

Two hundred thirty-five patients underwent RF catheter abhtion of AV conduction for symptomatic drug refractoiy AF (84%), atrial flutter (9%), and atrial tachycardia (7%). In the first 100 patients, postahlation pacing was not prospectively set at any specific rate and was always ≤ 70 beats/min. In the next 135 patients, postabiotion pacing was prospectively set at 90 beats/min for 1–3 months. Six of the first 100 patients (6%) had VF or sudden death after the RF procedure and none (0%) of the next 135 patients did (P < 0.05). One of the six patients had recurrent VF 4 days after the ablation. Five patients were successfully resuscitated and one patient died. There were no statistically significant differences between patients with and without (aborted) sudden death or between the first 100 and the next 135 patients with respect to age, sex, underlying heart disease, EF, number of RF applications, or leftor right-sided approach of the procedure. VF mostly occurred during episodes of slow ventricular escape rhythms or during slow ventricular pacing. We conclude that malignant ventricular arrhythmias and sudden death are possible complications of RF ablation of the AV junction. The mechanism of these complications could have a bradycardia dependent nature and it seems that the occurrence of malignant arrhythmias can be prevented by temporarily pacing the heart at relatively fast rates immediately after ablation.

Antiarrhythmic drugs have systematically failed to improve--or have even worsened prognosis--when given prophylactically to "high-risk" patients without previous spontaneous sustained ventricular arrhythmias. In patients who have had > or = 1 episode(s) of near sudden cardiac death or sustained ventricular arrhythmias, randomized studies against placebo have been considered unethical. Therefore, no information exists on the value of treatment with antiarrhythmic drugs in the prevention of sudden death in these patients. Sudden death is quite predictable and almost expected in some situations. The number of "very high risk" patients is small, but the incidence of sudden death among them is very high. A prophylactic implantable cardioverter-defibrillator (ICD) can be easily justified in them. Unfortunately, the greatest absolute number of sudden deaths occurs in patients from a very large population with a rather low risk for sudden death. Truly unexpected cardiac death is most frequently caused by the first acute ischemic event in a previously asymptomatic individual. While the causes of sudden cardiac death are multiple, the final link is frequently the same: ventricular fibrillation. This arrhythmia can be effectively recognized and treated by an ICD, irrespective of its initiating cause. The time when an ICD will be given prophylactically to a truly asymptomatic individual may never come, but there is an urgent need to implant this device prophylactically in patients who are clearly at risk for sudden death. There are medical, ethical, statistical, technical, practical, financial, and even philosophical obstacles involved in the concept of a prophylactic ICD, but they can be solved, because this therapy is effective. Deciding on the benefits of a prophylactic ICD is a probabilistic issue analogous to deciding on mass vaccination against a preventable infection. To the political community, the decision to accept a prophylactic ICD is too much a matter of expenses, because the benefits may not seem that obvious to them. To the device industry, the cleaves between doctors and politicians have to be the best stimuli to come along with cost-effective technology acceptable to both sides.

Many criteria have been published to localize accessory pathways from the 12-lead ECG during sinus rhythm. This study analyzed whether the localization of an accessory pathway could be predicted by using the polarity of the QRS complex during sinus rhythm on the surface ECG, instead of the delta wave polarity as used in many reports. The ECGs of 140 patients with an overt and single accessory pathway were evaluated. Eight localizations were taken into account. The precise location was previously known from successful radiofrequency ablation sites. In 128 patients (92%), the new algorithm allowed an accurate diagnosis of the site of implantation of the accessory pathway. Analysis of the polarity of the QRS complex on five electrocardiographic leads provides an easy, fast and reliable way to localize accessory pathways during sinus rhythm.