Termination of desynchronization rhythm and restoration of cardiac resynchronization by left‐sided ventricular premature complexes

Cardiac resynchronization devices that sense left ventricular (LV) activity and can detect interruptions of resynchronization therapy are able to record all forms of desynchronization rhythms, which are triggered by misalignment of LV timing cycles. We report five cases of this desynchronization rhythm that were terminated by isolated left‐sided ventricular premature complexes (LVPC) undetected by the right ventricular (RV) channel and unaccompanied by changes in the duration of the RV pacing cycles. In three cases, the devices did not even sense the LVPCs responsible for desynchronization termination. The restoration of resynchronization in our cases is in contrast to the traditional termination mode that is invariably associated with changes in the duration of the RV cycles.     

Stereotactic body radiation therapy for refractory ventricular tachycardia secondary to cardiac lipoma: A case report

We present the case of a 29‐year‐old man who developed ventricular tachycardia (VT) secondary to a cardiac lipoma located adjacent to the interventricular groove, which could not be fully resected. Antiarrhythmic drugs and endocardial and epicardial ablation failed to prevent VT recurrence. Finally, noninvasive stereotactic body radiation therapy (SBRT) targeting the lipoma was performed, with a total dose of 24 Gy delivered in three fractions. The number of VT episodes was reduced from 189/24 h before SBRT to 0 after the procedure. At 4‐month follow‐up, there were no signs of therapy‐related complications. Our experience suggests that SBRT could emerge as a viable treatment option for patients with cardiac tumors who develop refractory ventricular arrhythmias.     

Diagnostic evaluation and arrhythmia mechanisms in survivors of unexplained cardiac arrest

Identifying the cause of unexplained cardiac arrest is critical for appropriate management of both survivors and their family members. Aborted cardiac arrests whose cause remains unknown following investigation with a surface ECG, echocardiogram, and coronary angiogram are deemed unexplained. Many of these unexplained arrests are felt to be secondary to concealed forms of cardiac channelopathies and latent or subtle cardiomyopathies. This recognition has led to evaluating a diagnostic role for a series of additional investigations, including advanced imaging, genetic testing, and provocative forms of testing, including sodium channel blockade and treadmill testing. Despite evidence of an improved diagnostic yield through their systematic usage, clinical guidelines have yet to endorse a formal algorithm delineating investigations that must be performed before assigning a label of idiopathic ventricular fibrillation, which has resulted in markedly variables thresholds for concluding this diagnosis. Debate remains regarding the need for an invasive electrophysiology study among these patients, though identification of arrhythmic culprits requiring intracardiac electrograms for diagnostic confirmation have suggested a potential role when an initial comprehensive evaluation is unrevealing. Although progress is being made, the sizeable portion of arrests that remain unexplained despite completion of a comprehensive evaluation highlights an ongoing need for further research and additional tools to help unravel the ongoing mysteries of these near fatal events.     

Accuracy of a predictive model for severe hepatic fibrosis or cirrhosis in chronic hepatitis C

AIM: To assess the accuracy of a model in diagnosing severe fibrosis/cirrhosis in chronic hepatitis C virus (HCV) infection. METHODS: The model, based on the sequential combination of the Bonacini score (BS: ALT/AST ratio, platelet count and INR) and ultrasonography liver surface characteristics, was applied to 176 patients with chronic HCV infection. Assuming a pre-test probability of 35%, the model defined four levels of post-test probability of severe fibrosis/cirrhosis: <10% (low), 10-74% (not diagnostic), 75-90% (high) and >90% (almost absolute). The predicted probabilities were compared with the observed patients' distribution according to the histology (METAVIR). RESULTS: Severe fibrosis/cirrhosis was found in 67 patients (38%). The model discriminated patients in three comparable groups: 34% with a very high (>90%) or low (<10%) probability of severe fibrosis, 33% with a probability ranging from 75% to 90%, and 33% with an uncertain diagnosis (i.e., a probability ranging from 10% to 74%). The observed frequency of severe fibrosis/ cirrhosis was within the predefined ranges. CONCLUSION: The model can correctly identify 67% of patients with a high (>75%) or low (<10%) probability of cirrhosis, leaving only 33% of the patients still requiring liver biopsy.     

The expanding clinical spectrum of Anderson-Fabry disease: a challenge to diagnosis in the novel era of enzyme replacement therapy

Anderson-Fabry disease is an X-linked recessive lysosomal storage disease resulting from deficient alpha-galactosidase A activity. The conception of the disease has changed within the last decade. Studies of the last years have shown that the disease is not limited to the classical full-blown manifestation in affected males, which is well known since more than a century, but may also occur in carrier females. The phenomenology may differ in severity and kind of organ manifestation. Cardiac and renal variants with solely disease manifestation of these organs have also been described in an increasing number. It is likely that a spectrum exists regarding alpha-galactosidase A activity in both genders on the one hand, and an additional one regarding the severity and the number of organs affected on the other. The purpose of this review is to sharpen physicians' perception of this disease. Early and accurate diagnosis is mandatory considering that this disorder is now, after introduction of the novel enzyme replacement therapy, a treatable disease.     

Threonine-17 phosphorylation of phospholamban: a key determinant of frequency-dependent increase of cardiac contractility

Multiple studies have shown that phospholamban (PLN) plays a key role in regulation of frequency-dependent increase of cardiac contraction, a hallmark of the contractile reserve in myocardium. However, the mechanisms underlying this relationship remain elusive. Phosphorylation of PLN occurs on residues: serine-16 (Ser(16)) and threonine-17 (Thr(17)) in vivo. In isolated wild-type cardiomyocytes, we found that increases of stimulation frequency from 0.5 to 5 Hz were associated with increased Thr(17) phosphorylation of PLN and cardiac contractility. To further delineate the role of PLN phosphorylation in the frequency-dependent increases of cardiac function, three transgenic mouse models, expressing wild-type, Ser16Ala (S16A), or Thr17Ala (T17A) mutant PLN in the null background were generated. Transgenic lines expressing similar levels of wild-type or mutant PLN were selected and isolated cardiomyocytes were paced from 0.5 to 5 Hz. Upon increases in pacing frequency, the fractional shortening (FS) and rates of contraction (+dL/dt) and relaxation (-dL/dt) increased in wild-type and S16A mutant PLN cardiomyocytes. In contrast, in myocytes expressing the T17A mutant PLN, there were no increases in FS and +/-dL/dt upon increasing the frequency of stimulation. The time to 50% peak shortening (TTP(50)) and to 50% relaxation (TTR(50)) were also abbreviated to a much higher extent (two-fold) in wild-type and S16A mutant compared to T17A mutant PLN cardiomyocytes. These results indicate that Thr(17) phosphorylation of PLN is the major contributor to frequency-dependent increases of contractile and relaxation parameters in mouse cardiomyocytes, although some increases in these parameters occur even in the absence of PLN phosphorylation. Thus, the positive force-frequency relationship in cardiomyocytes is mechanistically and mainly related to PLN phosphorylation.     

Malnutrition in patients suffering from chronic heart failure; the nurse's care

Chronic heart failure is associated with a bad prognosis with considerably shortened survival and repeated hospitalisations. Patients suffering from heart failure also have symptoms that can affect their food intake, for example, tiredness when strained, breathing difficulties and gastrointestinal symptoms like nausea, loss of appetite and ascites. Pharmacological therapy can lead to a loss of appetite, which will make the intake of food inadequate to fill the required energy and nutritional needs. The nurse's interest in and knowledge of diet issues can improve these patients' nutritional status. The aim of this literature review was to describe the nurse's interventions regarding malnutrition in patients suffering from chronic heart failure. The literature search gave 13 articles, which were analysed, and sentences whose content was related to the aim were identified. Three areas of content appeared; drug treatment and consequences, gastrointestinal effects, and information and education. The results show that the nutritional status of these patients can be significantly improved by means of simple nursing interventions. Future research should focus on controlled experimental studies to evaluate differences in body weight, body mass index and quality of life between patients suffering from chronic heart failure, who are taking part in a fully enriched nutrition intervention, and patients suffering from chronic heart failure, who are eating their normal diet.     

Acute changes in blood pressure as a cause of cardiac arrhythmias

The effect of an acute change in blood pressure (BP) on ventricularectopic activity and the influence of antiarrhythmic agentson this effect were examined in 24 patients. In 11 patientswith premature ventricular complexes (PVCs), the BP was temporarilyreduced by a sodium nitroprusside drip. In all of them the incidenceof PVCs was reduced (or annihilated) by the induced hypotension.In 13 patients without ventricular ectopic activity, a metaraminoldrip was given until either a PVC appeared or the systolic BPreached 200 mmHg, or symptoms appeared. In 12 cases at leastone PVC appeared and in 8 of them the total number of PVCs was13 or more, usually in the form of bigeminy. The repetitionof the test following quinidine administration (serum quinidinelevel 1.7 ±0.5 ng ml^–1) in 6 cases did not changethis pattern, with one exception. It prevented the appearanceof idioventricular accelerated rhythm in one case in whom thisrhythm had been induced by the hypertension provocative testbefore the quinidine administration. All cases, in whom thetest failed to induce more than 3 PVCs, had no cardiac problemat all. Six of the 8 cases in whom the test induced 13 or morePVCs had organic cardiac disease or palpitation. Other arrhythmiasobserved on BP elevation, were supraventricular extra beats,nodal escape rhythms and atrioventricular block. In one casewith cardiomyopathy, the BP elevation was associated with earlysigns of heart failure that subsided quickly. In conclusion, acute elevation on BP may be associated withthe generation of PVCs and its reduction with their reductionor disappearance.