Effective treatment of electrical storm by a wearable cardioverter defibrillator in a patient with severely impaired left ventricular function after myocardial infarction: a case report.

BACKGROUND: The implantation of cardioverter defibrillators (ICDs) is an established therapy in the prevention of sudden cardiac death in patients with systolic dysfunction after myocardial infarction. To avoid immediate implantation of an ICD, wearable cardioverter defibrillator vests (WCD) can be used to protect patients against malignant rhythm disorders, while at the same time drug-based heart failure therapy has to be initiated. This drug therapy can improve left ventricular ejection fraction and primary prophylactic cardioverter defibrillator implantation may not be necessary. However, the recent Vest Prevention of Early Sudden Death Trial (VEST) questioned the regular use of the WCD in this setting. CASE PRESENTATION: A 47-year-old Caucasian man with severely impaired left ventricular function early after myocardial infarction was prescribed a WCD as primary prophylaxis to prevent sudden cardiac death. Seven days after the patient was supplied with a WCD, the patient suffered from an electrical storm with recurrent ventricular tachycardia (VT), which was successfully terminated 17 times by the WCD. On coronary angiography, the formerly infarct-related right coronary artery had TIMI (Thrombolysis in Myocardial Ischemia Trial) III flow, and a remaining stenosis in the left anterior descending artery (LAD) was stented, which did not stop recurrent VT. In the electrophysiology (EP) study, a focus was mapped in the left inferior ventricle, which was ablated. This stopped the VT. A second radio-frequency (RF) ablation in the same area was necessary after 14 days. Finally, a permanent cardioverter defibrillator was implanted. CONCLUSION: We report the case of a patient who survived recurrent episodes of VT early after myocardial infarction by effective defibrillation with a WCD. The WCD is a useful device to bridge time until a final decision for implantation of a defibrillator.

Description of a novel RyR2 mutation in a juvenile patient with symptomatic catecholaminergic polymorphic ventricular tachycardia in sleep and during exercise: a case report.

BACKGROUND: Catecholaminergic polymorphic ventricular tachycardia is an inherited disease presenting with arrhythmic events during physical exercise or emotional stress. If untreated, catecholaminergic polymorphic ventricular tachycardia is a highly lethal condition: About 80% of affected individuals experience recurrent syncope, and 30% experience cardiac arrest. Catecholaminergic polymorphic ventricular tachycardia is caused by mutations in genes encoding ryanodine receptor type 2 (RyR2) and cardiac calsequestrin (CASQ2). In cases of sympathoadrenergic activation, both mutations result in a spontaneous Ca2+ release in cardiac cells, facilitating ventricular arrhythmias. CASE PRESENTATION: We present a case of a 17-year-old Caucasian boy who survived sudden cardiac death caused by ventricular fibrillation while performing running exercise in a fitness center. The diagnostic workup included blood tests, coronary angiography, electrophysiological testing, and cardiac magnetic resonance imaging, but all results were normal. Because the patient's medical history included recurrent syncope during physical and emotional stress, we strongly suspected catecholaminergic polymorphic ventricular tachycardia as the underlying disease. Genetic screening was performed and confirmed the diagnosis, revealing a new heterozygous point mutation in the gene for RyR2, c.12520T>A (p.F4174 l, exon 90, RyR2 gene). The patient was discharged from our hospital after undergoing implantation of an implantable cardioverter defibrillator for secondary prevention. Shortly after implantation, the implantable cardioverter defibrillator terminated a sustaining ventricular tachycardia episode by antitachycardic pacing. This episode occurred early in the morning while the patient was asleep. CONCLUSIONS: We present a case of catecholaminergic polymorphic ventricular tachycardia associated with a novel single point mutation in the RyR2 gene, which, to the best of our knowledge, has not been described in the literature so far. Our patient experienced arrhythmic events under both resting conditions and physical activity, an uncommon finding in patients with catecholaminergic polymorphic ventricular tachycardia. This novel mutation may cause arrhythmias independent of sympathoadrenergic stimulation, but further evidence is needed to prove causality.

Prediction of cardiovascular events after renal transplantation.

BACKGROUND: Pulse wave velocity (PWV) is a marker of arterial stiffness and predicts cardiovascular events in the nontransplantation population. Cardiovascular events (CVE) are the leading cause of death and one of the leading causes of graft failure in renal transplant recipients. The present prospective study investigates whether there is a correlation between PWV and CVE in renal transplant recipients. METHODS: A prospective study assessing the incidence of a composite cardiovascular endpoint within ≥ 3 years after pulse wave analysis was performed in 64 stable renal transplant recipients. Measurement of PWV, augmentation index (AI75), and aortic systolic pressure was conducted using the SphygmoCor (AtCor) device. The composite endpoint of the study was the incidence of either death, myocardial infarction, stroke, or admission for symptomatic intermittent claudication or decompensated congestive heart failure. RESULTS: Fifteen patients (23%) reached the composite endpoint during a follow-up of 4.4 years. Binary logistic regression using PWV, AI75, central aortic systolic pressure, peripheral systolic pressure, and pulse pressure as covariates revealed that PWV was significantly associated with cardiovascular events (10.1 ± 3.6 m/s in subjects reaching the endpoint vs 8.5 ± 1.5 m/s in subjects not reaching the endpoint; P = .048). CONCLUSION: Increased arterial stiffness as assessed by PWV predicts CVE in renal transplant recipients and may be regarded as a footprint of accelerated arteriosclerosis for those patients.

The impact of aerobic exercise on blood pressure variability.

There is increasing evidence that blood pressure variability (BPV, variation of blood pressure over time) constitutes a strong and independent marker of cardiovascular risk. The all-cause mortality is >50% greater in subjects with a standard deviation of inter-visit blood pressure >5 mm Hg. Regular aerobic exercise reduces blood pressure and is recommended by current hypertension guidelines as a basic lifestyle modification. It remains elusive, however, whether aerobic exercise is able to reduce BPV as well. In total, 72 hypertensive subjects were randomly assigned to an 8-12-week treadmill exercise program (target lactate 2.0±0.5 mmol l(-1)) or sedentary control. Blood pressure was measured by 24 h-ambulatory blood pressure monitoring (ABP). Two aspects of BPV were assessed: the variability of ABP and the variability of blood pressure on exertion. The coefficient of variation (CV) was used as a statistical measure of BPV. The CV of systolic daytime ABP was defined as primary outcome. The exercise program significantly decreased systolic and diastolic daytime ABP by 6.2±10.2 mm Hg (P<0.01) and 3.0±6.3 mm Hg (P=0.04), respectively. Moreover, it reduced blood pressure on exertion and increased physical performance (P<0.05 each). Exercise had no impact, however, on the CV of daytime (10.2±2.7 vs. 9.8±2.6%, P=0.30) and night-time systolic (8.9±3.2 vs. 10.5±4.1%, P=0.10) and diastolic ABP (daytime 11.5±3.3 vs. 11.5±3.1%, night-time 12.0±4.3 vs. 13.8±5.2%; P>0.05 each). Regular aerobic exercise is a helpful adjunct to control blood pressure in hypertension, but it has no effect on 24 h- BPV, an independent predictor of cardiovascular risk.

Calprotectin and neutrophil gelatinase-associated lipocalin in the differentiation of pre-renal and intrinsic acute kidney injury.

BACKGROUND: Urinary calprotectin has recently been identified as a promising biomarker for the differentiation of pre-renal and intrinsic acute kidney injury (AKI). This study compares the diagnostic performance of calprotectin and neutrophil gelatinase-associated lipocalin (NGAL) in this differential diagnosis. METHODS: Urinary calprotectin and NGAL concentrations were assessed in a study population of 87 subjects including 38 cases of intrinsic AKI, 24 cases of pre-renal AKI and 25 healthy controls. Urinary tract obstruction, renal transplantation and metastatic cancer were defined as exclusion criteria. RESULTS: Mean calprotectin concentrations were significantly lower in pre-renal (190.2 ± 205.7 ng mL(-1) ) than in intrinsic AKI (6250.1 ± 7167.2 ng mL(-1) , P < 0.001). Receiver-operating characteristic (ROC) analysis provided an AUC of 0.99. Mean NGAL concentrations were significantly higher in intrinsic than in pre-renal AKI as well (458.1 ± 695.3 vs. 64.8 ± 62.1 ng mL(-1) , P = 0.001) providing an AUC of 0.82. A combination of the present study population with the cohort of the proof of concept study led to a population of 188 subjects (58 pre-renal AKI, 90 intrinsic AKI, 40 healthy controls). ROC analyses provided an AUC of 0.97 for calprotectin and 0.76 for NGAL yielding sensitivity and specificity values of 93.3 and 94.8% (calprotectin) vs. 75.3 and 72.4% (NGAL). Optimal cut-off values were 440 ng mL(-1) (calprotectin) and 52 ng mL(-1) (NGAL). Pyuria increased calprotectin concentrations independent of renal failure. CONCLUSION: This study shows that both calprotectin and NGAL are able to differentiate between pre-renal and intrinsic AKI after exclusion of pyuria. In the present population, calprotectin presents a higher sensitivity and specificity than NGAL.

Prophylaxis of recurrent urinary tract infection after renal transplantation by cranberry juice and L-methionine.

BACKGROUND: Recurrent urinary tract infections (UTIs) increase mortality and reduce graft survival after renal transplantation. Strategies to prevent recurrent UTIs include L-methionine, cranberry juice, and antibiotics. Data on the efficacy of cranberry and L-methionine, however, are controversial in the general population; there are few data in renal transplant recipients. METHODS: We performed a retrospective analysis of 82 transplant recipients with recurrent UTIs, who underwent prophylaxis with cranberry juice (2 × 50 mL/d, n = 39, 47.6%), or L-methionine (3 × 500 mg/d, n = 25, 30.5%), or both modalities (n = 18, 21.9%). Thirty patients without prophylaxis served as controls. We analyzed symptoms, pyuria/nitrituria, and incidence of UTI events during 1 year before versus after initiation of prophylaxis. RESULTS: Prophylaxis highly significantly decreased the annual UTI incidence by 58.3% (P < .001) in the study population with no change in the control group (P = .85); in addition, 53.7% of symptomatic patients reported relief of symptoms and pyuria/nitrituria disappeared in 42.4% of the dipstick-positive patients (P < .001 each). Cranberry reduced the annual number of UTI episodes by 63.9% from 3.6 ± 1.4 to 1.3 ± 1.3/year (P < .001) and L-methionine by 48.7% from 3.9 ± 1.8 to 2.0 ± 1.3/year (P < .001). CONCLUSION: Cranberry juice and L-methionine successfully reduced the incidence of UTI after renal transplantation.

Does external counterpulsation augment mean cerebral blood flow in the healthy brain? Effects of external counterpulsation on middle cerebral artery flow velocity and cerebrovascular regulatory response in healthy subjects.

BACKGROUND AND PURPOSE: External counterpulsation (ECP) noninvasively improves myocardial and organ perfusion via diastolic augmentation. The effects on cerebral blood flow velocities (CBFV) and hemodynamics are controversial. In this study, the effect of active ECP treatment on CBF in healthy subjects was continuously measured. METHODS: In 9 healthy volunteers (mean age 34.1 ± 11.1 years, 4 females), 20-min active ECP treatment was performed. CBFV in the middle cerebral artery were detected via transcranial Doppler. CBFV were registered continuously before, during and after ECP. The protocol was repeated twice. RESULTS: At onset of ECP, immediate changes in CBFV were observed: peak diastolic blood flow velocities increased from baseline to treatment (63 vs. 76 cm/s; p < 0.001) and diastolic blood flow augmentation was maintained throughout ECP. Peak systolic (87 vs. 78 cm/s; p < 0.001) and end-diastolic velocities (40 vs. 28 cm/s; p < 0.001) decreased significantly, while mean CBFV maintained constant (59 vs. 58 cm/s; not significant). The pulsatility index and resistance index as indirect parameters for peripheral vascular resistance increased during ECP (pulsatility index 0.79 vs. 0.89, p < 0.001; resistance index 0.54 vs. 0.64; p < 0.001). CONCLUSIONS: ECP did not increase mean CBFV in healthy subjects even though peak diastolic CBFV were significantly augmented. Changes in CBFV and transcranial Doppler waveform characteristics suggest that the mean flow of the middle cerebral artery is maintained stable via cerebrovascular autoregulatory mechanisms.

Improvement of fractional flow reserve and collateral flow by treatment with external counterpulsation (Art.Net.-2 Trial).

BACKGROUND: Arteriogenesis (collateral artery growth) is nature's most efficient rescue mechanism to overcome the fatal consequences of arterial occlusion or stenosis. The goal of this trial was to investigate the effect of external counterpulsation (ECP) on coronary collateral artery growth. MATERIALS AND METHODS: A total of 23 patients (age 61 +/- 2.5 years) with stable coronary artery disease and at least one haemodynamic significant stenosis eligible for percutaneous coronary intervention were prospectively recruited into the two study groups in a 2 : 1 manner (ECP : control). One group (ECP group, n = 16) underwent 35 1-h sessions of ECP in 7 weeks. In the control group (n = 7), the natural course of collateral circulation over 7 weeks was evaluated. All patients underwent a cardiac catheterization at baseline and after 7 weeks, with invasive measurements of the pressure-derived collateral flow index (CFIp, primary endpoint) and fractional flow reserve (FFR). RESULTS: In the ECP group, the CFIp (from 0.08 +/- 0.01 to 0.15 +/- 0.02; P < 0.001) and FFR (from 0.68 +/- 0.03 to 0.79 +/- 0.03; P = 0.001) improved significantly, while in the control group no change was observed. Only the ECP group showed a reduction of the Canadian Cardiovascular Society (CCS, P = 0.008) and New York Heart Association (NYHA, P < 0.001) classification. CONCLUSION: In this study, we provide direct functional evidence for the stimulation of coronary arteriogenesis via ECP in patients with stable coronary artery disease. These data might open a novel noninvasive and preventive treatment avenue for patients with non-acute vascular stenotic disease.