Diastolic dysfunction precedes myocardial hypertrophy in the development of hypertension

Background: Left ventricular (LV) hypertrophy and impaired diastolic function may occur early in systemic hypertension, but longitudinal studies are missing. Methods: We performed an echocardiographic follow-up study in young initially normotensive male offspring of hypertensive (OHyp) (n = 25) and normotensive (ONorm) (n = 17) parents. Blood pressure (BP), LV mass, and mitral inflow were determined at baseline and after 5 years. Pulmonary vein flow pattern assessment and septal myocardial Doppler imaging were additionally performed at follow-up. Results: At follow-up, BP was not significantly different between the two groups (128 ± 11 / 84 ± 10 v 123 ± 11 / 81 ± 5 mm Hg, OHyp v ONorm) but five OHyp had developed mild hypertension. LV mass index remained unchanged and was not different between the two groups at follow-up (92 ± 17 v 92 ± 14 g/m2). Diastolic echocardiographic properties were similar at baseline, but, at follow-up, the following differences were found: mitral E deceleration time (209 ± 32 v 185 ± 36 msec, P < .05) and pulmonary vein reverse A wave duration (121 ± 15 v 107 ± 12 msec, P < .05) were prolonged in the OHyp as compared to the ONorm. Compared to the normotensive subjects, the five OHyp who developed hypertension had more pronounced alterations of LV diastolic function, that is, significantly higher mitral A (54 ± 7 v 44 ± 9 cm/sec, hypertensives v normotensives, P < .05), lower E/A ratio (1.31 ± 0.14 v 1.82 ± 0.48, P < .05), increased systolic-to-diastolic pulmonary vein flow ratio (1.11 ± 0.3 v 0.81 ± 0.16, P < .005), longer myocardial isovolumic relaxation time (57 ± 7 v 46 ± 12 msec, P < .05) as well as smaller myocardial E (10 ± 1 v 13 ± 2 cm/sec, P < .05) and E/A ratio (1.29 ± 0.25 v 1.78 ± 0.43, P < .05), despite similar LV mass (91 ± 16 v 93 ± 18 g/m2). Conclusion: Over a 5-year follow-up, initially lean, normotensive, young men with a moderate genetic risk for hypertension, developed Doppler echocardiographic alterations of LV diastolic function compared to matched offspring of normotensive parents. These alterations were more pronounced in the OHyp who developed mild hypertension and occurred without a distinct rise in LV mass. Am J Hypertens 2001;14:106-113 © 2001 American Journal of Hypertension, Lt

An indicator of sudden cardiac death during brief coronary occlusion: electrocardiogram QT time and the role of collaterals

Aims The coronary collateral circulation has a beneficial role regarding all-cause and cardiac mortality. Hitherto, the underlying mechanism has not been clarified. The aim of this prospective study was to assess the effect of the coronary collateral circulation on electrocardiogram (ECG) QTc time change during short-term myocardial ischaemia. Methods and results A total of 150 patients (mean age 63 ± 11 years, 38 women) were prospectively included in this study. An ECG was recorded at baseline and during a standardized 1 min coronary balloon occlusion. QT interval was measured before, during, and after balloon occlusion and was corrected for heart rate (QTc). Simultaneously obtained collateral flow index (CFI), expressing collateral flow relative to normal anterograde flow, was determined based on intracoronary pressure measurements. During occlusion of the left anterior descending coronary artery mean QTc interval increased from 422 ± 33 to 439 ± 36 ms (P < 0.001), left circumflex occlusion led to an increase from 414 ± 32 to 427 ± 27 ms (P < 0.001). QTc was not influenced by occlusion of the right coronary artery (RCA) (417 ± 35 and 415 ± 34 ms, respectively; P = 0.863). QTc change during occlusion of the left coronary artery was inversely correlated with CFI (R2 = 0.122, P = 0.0002). Conclusion Myocardial ischaemia leads to QT prolongation during a controlled 1 min occlusion of the left, but not the RCA. QT prolongation is inversely related to collateral function indicating a protective mechanism of human coronary collaterals against cardiac deat

A novel SCN5A mutation, F1344S, identified in a patient with Brugada syndrome and fever-induced ventricular fibrillation

Objective Brugada syndrome (BS) is an inherited electrical cardiac disorder characterized by right bundle branch block pattern and ST segment elevation in leads V1 to V3 on surface electrocardiogram that can potentially lead to malignant ventricular tachycardia and sudden cardiac death. About 20% of patients have mutations in the only so far identified gene, SCN5A, which encodes the α-subunit of the human cardiac voltage-dependent sodium channel (hNav1.5). Fever has been shown to unmask or trigger the BS phenotype, but the associated molecular and the biophysical mechanisms are still poorly understood. We report on the identification and biophysical characterization of a novel heterozygous missense mutation in SCN5A, F1344S, in a 42-year-old male patient showing the BS phenotype leading to ventricular fibrillation during fever. Methods The mutation was reproduced in vitro using site-directed mutagenesis and characterized using the patch clamp technique in the whole-cell configuration. Results The biophysical characterization of the channels carrying the F1344S mutation revealed a 10mV mid-point shift of the G/V curve toward more positive voltages during activation. Raising the temperature to 40.5°C further shifted the mid-point activation by 18mV and significantly changed the slope factor in Nav1.5/F1344S mutant channels from − 6.49 to − 10.27mV. Conclusions Our findings indicate for the first time that the shift in activation and change in the slope factor at a higher temperature mimicking fever could reduce sodium currents' amplitude and trigger the manifestation of the BS phenotyp

EHRA expert consensus statement on arrhythmic mitral valve prolapse and mitral annular disjunction complex in collaboration with the ESC Council on valvular heart disease and the European Association of Cardiovascular Imaging endorsed cby the Heart Rhythm Society, by the Asia Pacific Heart Rhythm Society, and by the Latin American Heart Rhythm Society.

peer reviewe

Bundle branch re-entry ventricular tachycardia in a patient with complete heart block

A 58-year-old male patient presented episodes of palpitations in the context of atrioventricular block treated by a dual-chamber pacemaker. Clinical and electrophysiological studies identified the tachyarrhythmia to be bundle branch re-entrant ventricular tachycardia, which was successfully treated by radiofrequency ablation of the proximal right bundle branch

Seasonal variations of ventricular arrhythmia clusters in defibrillator recipients

BACKGROUND: Clustering ventricular arrhythmias are the consequence of acute ventricular electrical instability and represent a challenge in the management of the growing number of patients with an implantable cardioverter-defibrillator (ICD). Triggering factors can rarely be identified. OBJECTIVES: Several studies have revealed seasonal variations in the frequency of cardiovascular events and life-threatening arrhythmias, and we sought to establish whether seasonal factors may exacerbate ventricular electrical instability leading to arrhythmia clusters and electrical storm. METHODS: Two hundred and fourteen consecutive defibrillator recipients were followed-up during 3.3 +/- 2.2 years. Arrhythmia cluster was defined as the occurrence of three or more arrhythmic events triggering appropriate defibrillator therapies within 2 weeks. Time intervals between two clusters were calculated for each month and each season, and were compared using Kruskal-Wallis test and Wilcoxon-Mann-Whitney test with Bonferroni adjustment. RESULTS: During a follow-up of 698 patient years, 98 arrhythmia clusters were observed in 51 patients; clustering ventricular arrhythmias were associated with temporal variables; they occurred more frequently in the winter and spring months than during the summer and fall. Accordingly, the time intervals between two clusters were significantly shorter during winter and spring (median and 95% CI): winter 16 (5-19), spring 11.5 (7-25), summer 34.5 (15-55), fall 50.5 (19-65), P = 0.0041. CONCLUSION: There are important seasonal variations in the incidence of arrhythmia clusters in ICD recipients. Whether these variations are related to environmental factors, change in physical activity, or psychological factors requires further study

Inappropriate interventions during the long-term follow-up of patients with an implantable defibrillator

QUESTIONS UNDER STUDY: In patients with an implantable defibrillator (ICD), inappropriate ICD interventions alter the quality of life, may cause hospitalisations and limit cost-effectiveness. The aim of the study was to determine the incidence and causes of inappropriate ICD interventions, and to identify patients at risk. METHODS: For this observational longitudinal study, consecutive patients undergoing ICD implantation at the University Hospital of Berne were included in a registry. All stored electrograms of episodes triggering ICD interventions were systematically reviewed and analysed to determine whether ICD interventions were appropriate or inappropriate. Inappropriate ICD interventions were classified according to their cause, and risk factors were sought. RESULTS: 214 consecutive patients were followed during a median time of 2.7 years (3.7 years IQR, 698 patient years). 81 inappropriate ICD interventions occurred in 58 patients (27%). Factors triggering inappropriate ICD interventions included atrial fibrillation and flutter (n = 35, 44%), sinus tachycardia (n = 26, 32%), lead fracture (n = 12), recurrent self-terminating ventricular tachycardia (n = 5), double-counting due to T-wave oversensing (n = 3). The only identifiable risk factor for inappropriate ICD interventions was sustained ventricular tachycardia as index arrhythmia. CONCLUSIONS: An important proportion of ICD patients suffer inappropriate ICD interventions that are most commonly due to supraventricular arrhythmias. Patients with ventricular tachycardia prior to ICD implantation are at higher risk of inappropriate ICD interventions. Interventions aiming at decreasing the risk of inappropriate ICD interventions should be considered in these patients