Dehydration with high natriuretic peptide levels! A word of caution.

B-type natriuretic peptide is secreted primarily by cardiomyocytes in response to increased ventricular or atrial wall stress reflecting volume or pressure overload. The relationship between natriuretic peptides and the severity of heart failure is well established. We present here a case where natriuretic peptide levels were increased due to dehydration in the abscence of renal impairment. Normalization of natriuretic peptide level was achieved by stopping the diuretics and the administration of normal saline.

Exercise related ventricular arrhythmias are related to cardiac fibrosis in hypertrophic cardiomyopathy mutation carriers.

AIMS: Hypertrophic cardiomyopathy (HCM) is a frequent cause of sudden cardiac death (SCD) due to exercise-related ventricular arrhythmias (ERVA); however the pathological substrate is uncertain. The aim was to determine the prevalence of ERVA and their relation with fibrosis as determined by cardiac magnetic resonance imaging (CMR) in carriers of an HCM causing mutation. METHODS: We studied the prevalence and origin of ERVA and related these with fibrosis on CMR in a population of 31 HCM mutation carriers. RESULTS: ERVA occurred in seven patients (23%) who all showed evidence of fibrosis (100% ERVA(+) vs. 58% ERVA(-), p = 0.04). No ventricular tachycardia or ventricular fibrillation occurred. In patients with ERVA, the extent of fibrosis was significantly larger (8 ± 4% vs. 3 ± 4%, p = 0.02). ERVA originated from areas with a high extent of fibrosis or regions directly adjacent to these areas. CONCLUSIONS: ERVA in HCM mutation carriers arose from the area of fibrosis detected by CMR; ERVA seems closely related to cardiac fibrosis. Fibrosis as detected by CMR should be evaluated as an additional risk factor to further delineate risk of SCD in carriers of an HCM causing mutation.

Unmappable ventricular tachycardia after an old myocardial infarction. Long-term results of substrate modification in patients with an implantable cardioverter defibrillator.

PURPOSE: The frequent occurrence of ventricular tachycardia can create a serious problem in patients with an implantable cardioverter defibrillator. We assessed the long-term efficacy of catheter-based substrate modification using the voltage mapping technique of infarct-related ventricular tachycardia and recurrent device therapy. METHODS: The study population consisted of 27 consecutive patients (age 68 ± 8 years, 25 men, mean left ventricular ejection fraction 31 ± 9%) with an old myocardial infarction and multiple and/or hemodynamically not tolerated ventricular tachycardia necessitating repeated device therapy. A total of 31 substrate modification procedures were performed using the three-dimensional electroanatomical mapping system. Patients were followed up for a median of 23.5 (interquartile range 6.5-53.2) months before and 37.8 (interquartile range 11.7-71.8) months after ablation. Antiarrhythmic drugs were not changed after the procedure, and were stopped 6 to 9 months after the procedure in patients who did not show ventricular tachycardia recurrence. RESULTS: Median ventricular tachycardias were 1.6 (interquartile range 0.7-6.7) per month before and 0.2 (interquartile range 0.00-1.3) per month after ablation (P = 0.006). Nine ventricular fibrillation episodes were registered in seven patients before and two after ablation (P = 0.025). Median antitachycardia pacing decreased from 1.6 (interquartile range 0.01-5.5) per month before to 0.18 (interquartile range 0.00-1.6) per month after ablation (P = 0.069). Median number of shocks decreased from 0.19 (interquartile range 0.04-0.81) per month before to 0.00 (interquartile range 0.00-0.09) per month after ablation (P = 0.001). One patient had a transient ischemic attack during the procedure, and another developed pericarditis. Nine patients died during follow-up, eight patients due to heart failure and one patient during valve surgery. CONCLUSION: Catheter-based substrate modification using voltage mapping results in a long-lasting reduction of cardioverter defibrillator therapy in patients with multiple and/or hemodynamically not tolerated infarct-related ventricular tachyarrhythmia.

Semi-final masked hypertension.

Masked hypertension is normal blood pressures (BP) in a clinical setting and high BP during ambulatory monitoring. Although these patients are at higher cardiovascular risk, there is still no clear consensus definition of masked hypertension.

A rare coronary anomaly: one ostium fits all.

Coronary anomalies affect a small percentage of the general population. A solitary coronary ostium in the absence of other major congenital anomalies is very rare. We describe a case of a patient, admitted to our cardiology department with an acute myocardial infarction. A coronary angiogram shows a solitary ostium originating from the right sinus of Valsalva with the left anterior descending coronary artery (LAD) ventral to the pulmonary artery and the circumflex artery (Cx) following its course retroaortically. The theoretical variant of this type of malformation has been described but has not been reported in a clinical case before. Coronary anomalies are usually detected during coronary angiography, but exact course determination and relationships are difficult to visualize. The use of cardiac computed tomography (CCT) allows visualization of the coronary anatomy in a 3-dimensional image and demonstrated an added value to coronary angiography.

Campylobacter jejuni: enterocolitis and myopericarditis.

Campylobacter jejuni enteritis is the commonest enteric infection in the developed world. There are only few reported cases in the medical literature of cardiac complications associated with C. jejuni enterocolitis, most of the patients in the reported literature were males and most of the cases followed a benign course. Severe left ventricular dysfunction complicated only two cases of C. jejuni myocarditis. We report here a young male with Campylobacter myopericarditis. We believe that this is the first reported case of Campylobacter associated myopericarditis in The Netherlands. The mechanism by which Campylobacter causes myo(peri)carditis remains uncertain, it may be caused by direct bacterial invasion of cardiac tissue, bacterial toxins, circulating immune complexes, or cytotoxic T-cells. Since the number of C. jejuni infection is increasing worldwide, cardiac complications, although rare, are a remarkable manifestation of this pathogen and should be always kept in mind.

Superior vena cava syndrome as a complication of colon carcinoma.

Superior vena cava syndrome is a group of signs and symptoms resulting from the impairment of blood flow through the SVC into the right atrium. We present a case of a 54-year-old female with superior vena cava syndrome due to metastasis of colon carcinoma into the SVC leading to an intraluminal obstruction. To our knowledge this is the first published report of an intraluminal metastasis of colon adenocarcinoma into the superior vena cava causing SVC syndrome.

Purulent pericarditis, an uncommon entity in modern practice: a case report.

We report an 82-year-old female with pneumococcal pneumonia. Antimicrobial therapy was started in an early stage of the disease. On the 10th day of admission she developed peripheral pitting oedema with elevated jugular venous pressure and a drop in blood pressure. Her electrocardiogram showed sinus tachycardia and concave upward ST-segment elevation in almost all leads. A transthoracic two-dimensional echocardiogram revealed a large circumferential pericardial effusion, with diastolic collapse of the right atrium and a mitral inflow pattern that suggested cardiac tamponade. Emergency pericardiocentesis was performed, releasing 600 cc of thick green purulent material, followed by good haemodynamic recovery. The haemodynamic state, pneumonic infiltrate and inflammatory parameters responded gradually to antimicrobial therapy and the patient recovered and was discharged after six weeks. We conclude that even susceptible strains of Streptococcus pneumonia in a patient with no predisposing factors may still cause purulent pericarditis, even in the era of adequate antibiotic therapy.