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PubMed1986

Atrial demand pacing to protect against vagal overactivity in sympathetic autonomic neuropathy.

The clinical features, investigation and management of a patient with a subacute autonomic neuropathy are described. A series of physiological and biochemical studies indicated severe but selective sympathetic cardiovascular dysfunction, associated with bradycardia. The bradycardia was enhanced by raising blood pressure but there was no other evidence either of cardiac vagal impairment or hyperreactivity. Oral atropine prevented the bradycardia but had to be withdrawn because of intolerable side effects. An atrial demand pacemaker was implanted to elevate basal heart rate and prevent bradycardia. The pacemaker alone did not improve postural hypotension but it enabled the blood pressure to be readily and safely controlled by a combination of drugs.

Autonomic Nervous System↗
PubMed2001

Differences in heart rate variability parameters during the post-dialytic period in type II diabetic and non-diabetic ESRD patients.

BACKGROUND: Heart rate variability parameters were evaluated in 10 healthy subjects, 10 type II diabetic patients and 20 end-stage renal disease (ESRD) patients (11 non-diabetic and nine type II diabetic) undergoing chronic haemodialysis. The study was divided in two phases. METHODS: In the first phase all subjects underwent electrocardiograph (ECG) recording under baseline conditions. In the second phase only ESRD patients underwent haemodialysis and ECG recording. On the day of dialysis and ECG recording the ECG recording was started 1 h before the haemodialysis session (pre-dialytic period), and continued throughout the dialysis (dialytic period), until the morning after (post-dialytic period). RESULTS: Compared with ESRD patients, non-ESRD patients showed the lowest cardiac sympathetic activity. Diabetic patients compared to non-diabetic patients showed a prevalence of cardiac sympathetic activity in the pre-dialytic period (P < 0.01). During the dialytic period in comparison with the pre-dialytic one, a further increase in cardiac sympathetic activity was observed in both diabetic and non-diabetic ESRD patients (P < 0.001). However, in the post-dialysis period the cardiac autonomic nervous system activity remained at the pre-dialytic condition in the diabetic group. In contrast, in the non-diabetic group the cardiac autonomic balance shifted towards a parasympathetic prevalence in the post-dialytic period (P < 0.01). In addition, a significant correlation was found between changes in heart rate variability and changes in plasma urea concentration in the non-diabetic group only (r = 0.65; P < 0.03). CONCLUSIONS: Non-insulin-dependent diabetic uraemic patients undergoing a chronic haemodialysis programme have a severe impairment of heart rate variability. This is probably due to autonomic neuropathy related to the effects of both diabetes and chronic uraemic conditions. In non-diabetic haemodialysis patients uraemia causes similar but reversible changes in heart rate variability compared with the changes caused by diabetes.

Autonomic Nervous System↗
PubMed1994

Demonstration of entrainment and presence of slow conduction during ventricular tachycardia in arrhythmogenic right ventricular dysplasia.

During VT in two cases with arrhythmogenic right ventricular dysplasia, entrainment criteria, constant fusion beats except for the last entrainment beat, progressive fusion, and a localized conduction block associated with interruption of VT, were demonstrated with rapid ventricular pacing performed during VT. Furthermore, a long conduction interval was present during entrainment from the pacing site to the earliest activation site during VT, indicating the presence of a slow conduction area. VT in these cases was, thus, due to reentry with an area of slow conduction within the circuit.

Action Potentials↗
PubMed1999

Cardiac autonomic responses to volume overload in normal subjects and in patients with dilated cardiomyopathy.

This study evaluated the effects of acute isotonic volume expansion on heart rate variability (HRV) in 10 patients with dilated cardiomyopathy (DCM) and in 10 age- and sex-matched normal volunteers. Echocardiographic left ventricular volumes and HRV measurements by continuous Holter recording were assessed at baseline, at 60 and 120 min during intravenous saline load (0.9% NaCl, 0.25 ml. kg(-1). min(-1)), and 60 min after infusion was terminated. Data analysis was performed by repeated-measures ANOVA. After volume expansion, left ventricular ejection fraction increased (F = 9.8; P < 0.001) in normal subjects and decreased (F = 8.7; P < 0.001) in DCM patients. During volume expansion a significant difference was also detectable between the two groups in root-mean-square successive difference (F = 25.2; P < 0.001), percentage of differences between successive normal R-R intervals >50 ms (F = 97.6; P < 0.001), high-frequency power (F = 50.1; P < 0.001), and low-frequency power (F = 41.6; P < 0.001), all of which reflect parasympathetic modulation of heart rate; in fact, these measurements increased in normal subjects and decreased in DCM patients. In normal subjects, the increase in HRV measurements during volume expansion suggests a parasympathetic activation, mediated by stimulation of cardiopulmonary and arterial mechanoreceptors. On the contrary, in DCM patients the parasympathetic withdrawal, already detectable at baseline, increases during volume expansion.

Adult↗
PubMed2000

Role of the endothelial glycocalyx in dromotropic, inotropic, and arrythmogenic effects of coronary flow.

Coronary flow regulates cardiac functions, and it has been suggested that endothelial membrane glycosylated proteins are the primary shear stress mechanosensors. Our hypothesis was that if these proteins are the sensors for flow, then intracoronary perfusion of lectins or specific antibodies should differentially depress coronary flow-enhanced responses of different parenchymal cell types such as auricular-ventricular (A-V) nodal cells (dromotropic effect), contractile myocytes (inotropic effect), and junctional Purkinje-muscle cells (spontaneous ventricular rhythm). The coronary flow stimulatory effects on A-V delay and spontaneous ventricular rhythm were selectively depressed by six of eight lectins. None of the lectins depressed the coronary flow inotropic effect. Antibodies against endothelial surface proteins, alpha(v)beta(5)-integrin and sialyl-Lewis(b) glycan, depressed the dromotropic but not the inotropic effects of coronary flow, whereas the vascular cell adhesion molecule 1 antibody had no effect on the dromotropic, but enhanced the inotropic, effect. The fact that lectins and antibodies differentially depressed regional coronary flow effects suggests that there is a chemical distinctiveness in their intravascular endothelial cell surfaces. However, nonselective cross-linking of endothelial glycocalyx proteins with 2,000-kDa dextran-aldehyde or vitronectin indistinctively depressed the dromotropic and inotropic effects of coronary flow. These results indicate that coronary flow-induced stress acts on specific structures located in the capillary intravascular membrane glycocalyx.

Aldehydes↗
PubMed2001

Depression, heart rate variability, and acute myocardial infarction.

BACKGROUND: Clinical depression is associated with an increased risk for mortality in patients with a recent myocardial infarction (MI). Reduced heart rate variability (HRV) has been suggested as a possible explanation for this association. The purpose of this study was to determine if depression is associated with reduced HRV in patients with a recent MI. METHODS AND RESULTS: Three hundred eighty acute MI patients with depression and 424 acute MI patients without depression were recruited. All underwent 24-hour ambulatory electrocardiographic monitoring after hospital discharge. In univariate analyses, 4 indices of HRV were significantly lower in patients with depression than in patients without depression. Variables associated with HRV were then compared between patients with and without depression, and potential confounds were identified. These variables (age, sex, diabetes, and present cigarette smoking) were entered into an analysis of covariance model, followed by depression status. In the final model, all but one HRV index (high-frequency power) remained significantly lower in patients with depression than in patients without depression. CONCLUSIONS: We conclude that greater autonomic dysfunction, as reflected by decreased HRV, is a plausible mechanism linking depression to increased cardiac mortality in post-MI patients.

Autonomic Nervous System↗
PubMed2005

Regional differences in APD restitution can initiate wavebreak and re-entry in cardiac tissue: a computational study.

BACKGROUND: Regional differences in action potential duration (APD) restitution in the heart favour arrhythmias, but the mechanism is not well understood. METHODS: We simulated a 150 x 150 mm 2D sheet of cardiac ventricular tissue using a simplified computational model. We investigated wavebreak and re-entry initiated by an S1S2S3 stimulus protocol in tissue sheets with two regions, each with different APD restitution. The two regions had a different APD at short diastolic interval (DI), but similar APD at long DI. Simulations were performed twice; once with both regions having steep (slope > 1), and once with both regions having flat (slope < 1) APD restitution. RESULTS: Wavebreak and re-entry were readily initiated using the S1S2S3 protocol in tissue sheets with two regions having different APD restitution properties. Initiation occurred irrespective of whether the APD restitution slopes were steep or flat. With steep APD restitution, the range of S2S3 intervals resulting in wavebreak increased from 1 ms with S1S2 of 250 ms, to 75 ms (S1S2 180 ms). With flat APD restitution, the range of S2S3 intervals resulting in wavebreak increased from 1 ms (S1S2 250 ms), to 21 ms (S1S2 340 ms) and then 11 ms (S1S2 400 ms). CONCLUSION: Regional differences in APD restitution are an arrhythmogenic substrate that can be concealed at normal heart rates. A premature stimulus produces regional differences in repolarisation, and a further premature stimulus can then result in wavebreak and initiate re-entry. This mechanism for initiating re-entry is independent of the steepness of the APD restitution curve.

Action Potentials↗
PubMed2006

Assessment of cardiac autonomic regulation and ventricular repolarization after off-pump coronary artery bypass grafting.

BACKGROUND: Altered autonomic regulation precipitates cardiac arrhythmias and increases the risk of sudden cardiac death. This risk is further increased by changes in ventricular repolarization. Autonomic regulation is deranged in patients after myocardial on-pump revascularization. We aimed to clarify how off-pump coronary artery bypass grafting (CABG) affects postoperative cardiac autonomic regulation and ventricular repolarization within 4 weeks after CABG. METHODS: Forty-two patients (mean age, 61.9 +/- 9.3 years; mean EURO score 2.6 +/- 1.9) were electively admitted for off-pump CABG. The electrocardiographic and respiratory waveform recordings were performed in the afternoon in the supine position for 10 minutes. Autonomic modulation was assessed using heart rate variability analysis. Power spectra were computed from 5-minute stable RR intervals using Fourier Transform analysis. Total power of spectra was defined in the range of 0.01 to 0.40 Hz, high-frequency power within 0.15 to 0.40 Hz, and low-frequency power within 0.04 to 0.15 Hz. Normalized power was defined as a ratio of power in each band/total power. The high- and low-frequency power as well as their normalized values indicated cardiac vagal and sympathetic modulation, respectively. Ventricular repolarization was assessed using QT interval, QT interval variability, and QT-RR interdependence analysis. QT intervals were determined from the beginning of the 5-minute segments. QT interval variability was evaluated by a T-wave template-matching algorithm. Pearson correlation between length of RR and QT interval was applied to study QT-RR characteristics. The results were tested for significance using the Fisher exact test, nonpaired t test, and analysis of variance; a P <.05 was considered significant. RESULTS: The frequency of arrhythmic events and heart rate increased from the fourth to the seventh postoperative day and returned to preoperative levels 4 weeks after CABG. Heart rate variability measures indicating autonomic modulation remained depressed even 4 weeks after the procedure. QT variability index increased from -1.2 +/- 0.5 to -0.8 +/- 0.4 on the fourth day after the operation (P <.05) and returned to -1.0 +/- 0.5 4 weeks after CABG (P = not significant). QT-RR correlation decreased from 0.41 to 0.23 (P <.05) and remained significantly impaired as long as 4 weeks after CABG. CONCLUSIONS: Observed faster heart rates until 1 week after off-pump CABG imply excessive adrenergic activation, which is comparable to on-pump CABG procedure rates. The results indicate profound autonomic derangement and loss of rate-dependent regulation after off-pump CABG even 4 weeks after operation. Restituted repolarization as assessed by QT variability index 4 weeks postoperatively corresponded with decreased frequency of rhythm disturbances 4 weeks after CABG. The loss of coupling between QT and RR intervals shows increased electrical instability postoperatively, which may serve as an additional promoter for postoperative arrhythmias, especially at higher heart rates.

Aged↗
PubMed1976

Initial vectors of ventricular premature beats and anterior fascicular conduction defects.

Vectorcardiographic studies on ventricular premature beats (VPB'S), occurring in records wherein the sinus beats were associated with an intraventricular conduction defect attributed to anterior fascicular delay or block, did not identify the exact site of a presumed reentry mechanism. The hypothesis that the orientation of the initial vectors of the VPB might reveal either anterograde or retrograde emergence from the anterior fasciulus iwth a reentry PVB was not strongly supported, although one or the other mechanism was compatible with the early vectors of certain VPBs. The VPBs revealed greater angular change on the spatial orientation of sequential early vectors (5--10--15 milliseconds) than occurred in sinus beats. Recurring VPBs, which appeared to casual visual inspection steriotyped in form, showed considerable variation in the orientation of the early vectors, indicating, in the cases studied, that VPBs, in the strictest sense, may be associated with differing initial entrance pathways to the myocardium and thus may be 'multiform'.

Adult↗
PubMed2004

Relationship between gastroesophageal reflux disease and myocardial ischemia. Effect of reflux on temporary activity of autonomic nervous system.

PURPOSE: Assessment of the gastroesophageal reflux disease (GERD) influence on myocardial ischemia and autonomic nervous system (ANS) activity. MATERIAL AND METHODS: In 50 patients with angiographically confirmed ischemic heart disease (IHD) in I-III CCS class, simultaneous 24-hour ECG and esophageal pH-metry monitoring was performed. We assessed: (1) GERD occurrence in patients with IHD, (2) influence of pathological reflux (PR) on myocardial ischemia--number and total duration of ST depression episodes in GERD and non-GERD patients, (3) temporary activity of ANS was determined according to the dynamics of spectral HRV (Heart Rate Variability) analysis components (LF, HF, VLF, LF/HF). RESULTS: 23 patients (46%) fullfilled the GERD criteria. Patients with GERD had significantly higher number of ST depression episodes (4.13 vs 2.85, p = 0.013) as well as longer total duration of ischemia (64.73 vs 35.2 min, p = 0.034). Spectral HRV analysis showed the significant decrease of LF/HF ratio (p < 0.035), which indicates the sympathovagal balance shift towards the parasympathetic system caused by PR. CONCLUSIONS: 1. GERD is frequent condition in patients with angiographically confirmed IHD. Coexistence of GERD may predispose to the myocardial ischemia. 2. Gastroesophageal reflux may cause the shift of sympathovagal balance towards its parasympathetic component. This mechanism may induce esophago-cardiac reflex, leading to diminished myocardial perfusion.

Adult↗
PubMed1993

[The diagnostic value of standard ECG methods, the cold-pressure test and Valsalva maneuver in idiopathic QT syndrome].

The idiopathic Long QT Syndrome is an infrequently occurring disorder. Affected patients usually show ECG alterations and are prone to syncope and sudden arrhythmic cardiac death. Adequate therapy with beta-blocking drugs may significantly improve the prognosis of affected patients. The early and precise diagnosis of the disorder therefore has major prognostic impact. This paper reports the diagnostic significance of standard ECG, exercise stress testing, ambulatory ECG monitoring, cold pressor test and Valsalva maneuver in 14 patients with Long QT Syndrome. The results were compared with those obtained in 14 healthy age matched volunteers. QTc duration was significantly longer in patients with Long QT Syndrome during standard 12-lead ECG at rest (489 +/- 55 ms versus < vs. > 412 +/- 25 ms, p < 0.005), exercise stress test (490 +/- 39 ms vs. 409 +/- 18 ms, p < 0.001), cold pressor test (512 +/- 45 ms vs. 407 +/- 19 ms, p < 0.001), Valsalva maneuver (497 +/- 49 vs. 407 +/- 18 ms, p < 0.001), minimal heart rate during 24-h of ambulatory ECG monitoring (482 +/- 69 ms vs. 402 +/- 22 ms, p < 0.01) and maximal heart rate during Holter monitoring (460 +/- 47 ms vs. 411 +/- 27 ms, p < 0.005). Four of 14 patients with Long QT Syndrome had pathological findings during ambulatory ECG monitoring (two patients showed short episodes of asymptomatic torsade de pointes tachycardia, one patient had an intermittent SA-Block, and one patient showed T-wave alternans). All healthy volunteers had normal ambulatory ECG recordings (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗