Incidence Of Premature Ventricular Complexes Research Articles

Calcium handling dysfunction and cardiac damage following acute ventricular preload challenge in the dystrophin-deficient mouse heart.

Duchenne muscular dystrophy (DMD) is the most common muscular dystrophy and is caused by mutations in the dystrophin gene. Dystrophin deficiency is associated with structural and functional changes of the muscle cell sarcolemma and/or stretch-induced ion channel activation. In this investigation, we use mice with transgenic cardiomyocyte-specific expression of the GCaMP6f Ca2+ indicator to test the hypothesis that dystrophin deficiency leads to cardiomyocyte Ca2+ handling abnormalities following preload challenge. α-MHC-MerCreMer-GCaMP6f transgenic mice were developed on both a wild-type (WT) or dystrophic (Dmdmdx-4Cv) background. Isolated hearts of 3-7-mo male mice were perfused in unloaded Langendorff mode (0 mmHg) and working heart mode (preload = 20 mmHg). Following a 30-min preload challenge, hearts were perfused in unloaded Langendorff mode with 40 μM blebbistatin, and GCaMP6f was imaged using confocal fluorescence microscopy. Incidence of premature ventricular complexes (PVCs) was monitored before and following preload elevation at 20 mmHg. Hearts of both wild-type and dystrophic mice exhibited similar left ventricular contractile function. Following preload challenge, dystrophic hearts exhibited a reduction in GCaMP6f-positive cardiomyocytes and an increase in number of cardiomyocytes exhibiting Ca2+ waves/overload. Incidence of cardiac arrhythmias was low in both wild-type and dystrophic hearts during unloaded Langendorff mode. However, after preload elevation to 20-mmHg hearts of dystrophic mice exhibited an increased incidence of PVCs compared with hearts of wild-type mice. In conclusion, these data indicate susceptibility to preload-induced Ca2+ overload, ventricular damage, and ventricular dysfunction in male Dmdmdx-4Cv hearts. Our data support the hypothesis that cardiomyocyte Ca2+ overload underlies cardiac dysfunction in muscular dystrophy.NEW & NOTEWORTHY The mechanisms of cardiac disease progression in muscular dystrophy are complex and poorly understood. Using a transgenic mouse model with cardiomyocyte-specific expression of the GCaMP6f Ca2+ indicator, the present study provides further support for the Ca2+-overload hypothesis of disease progression and ventricular arrhythmogenesis in muscular dystrophy.

Abstract 16545: Sinus Rhythm Dynamics and Ventricular Ectopy in an Experimental Model of Aging

Aging is coupled with alterations of heart rate and heart rate variability (HRV), together with increased incidence of arrhythmias and sudden cardiac death. But whether changes of sinus rhythm properties of the aged heart correlate with enhanced occurrence of ventricular ectopic discharge remains unclear. Thus, we studied the effects of aging on heart rate, HRV, and occurrence of premature ventricular complexes (PVCs) in aging C57Bl/6 mice. Electrocardiograms (ECG) were obtained in male and female conscious mice at ~4, ~12, ~18, and ~24 months of age (n=37-66). Heart rate was preserved at ~4, ~12, and ~18 months (729±30, 730±22, and 725±20 bpm) and reached a minimum at ~24 months (708±37 bpm). Standard deviation of RR intervals, an indicator of HRV, was maximal at ~4 months (3.5±1.7 ms) and was reduced at ~12, ~18, and ~24 months (2.6±1.5, 2.5±1.3, and 2.6±1.3 ms). By frequency domain analysis, high-frequency components of RR interval variations, indicative of parasympathetic influence, were preserved with aging. In contrast, low frequency components, comprising the influence of sympathetic and parasympathetic axis, were maximal in young animals and progressively decrease at ~12, ~18, and ~24 months. PVCs were observed in only 3% of mice at ~4 months, a fraction that increased to 11%, 10%, and 22% at ~12, ~18, and ~24 months, respectively. For each age interval, heart rate and HRV parameters for animals with PVCs were distributed within the range observed in mice not experiencing ventricular ectopy. Moreover, for animals with PVCs, parameters of HRV before the occurrence of ectopic beats were comparable to those observed during undisturbed sinus rhythm, although a tendency for lower heart rate was seen. To address the role of the autonomic nervous system on incidence of ectopic events, ECGs were collected before and after block of the sympathetic and parasympathetic axis in mice at ~4 months (n=30) and ~24 months (n=26). This intervention reduced heart rate in both groups of animals and attenuated HRV exclusively in young. Moreover, combine autonomic block decreased incidence of PVCs by 50% and 57% in young and old animals, respectively. Collectively, these results suggest that occurrence of ventricular ectopy does not correlate with heart rhythm dynamics.

Anti-arrhythmogenic and anti-inflammatory effects of troxerutin in ischemia/reperfusion injury of diabetic myocardium

IntroductionMedicinal plants are increasingly used in the treatment of cardiovascular diseases due to their multifaceted properties. This study was designed to investigate anti-arrhythmic and anti-inflammatory potentials of the natural bioflavonoid, troxerutin (TXR) in myocardial ischemia/reperfusion (I/R) injury in diabetic rats. MethodsMale Wistar rats were randomly divided into 4 groups (control, control + TXR [150 mg/kg, daily], diabetic, and diabetic + TXR). Type-1 diabetes was induced by an intraperitoneal injection of streptozotocin (50 mg/kg) and lasted for 10 weeks. After mounting on the Langendorff apparatus, isolated hearts in all groups received a normal Krebs–Henseleit solution for 20 min of stabilization period, followed by 30 min of regional ischemia through ligation of the left anterior descending coronary artery, and 60 min of full reperfusion. During the experiment, the electrocardiograms were recorded and the arrhythmias [number, duration and incidence of premature ventricular complexes (PVC), ventricular tachycardia (VT), ventricular fibrillation (VF), and arrhythmia score] during I/R phases were assessed based on the Lambeth Convention. Ischemic left ventricular samples were used to determine the activities of lactate dehydrogenase (LDH), interleukin-1beta (IL-1β), and tumor necrosis factor (TNF-α). ResultsThe arrhythmias induced by I/R were not significantly changed in diabetic group as compared to the control group. However, pretreatment with TXR significantly reduced the number of PVC and duration and incidence of VF in ischemic phase in comparison to the untreated animals (P < 0.05). In addition, the duration, and incidence of most arrhythmias during reperfusion phase were significantly declined by TXR administration in both control and diabetic groups (P < 0.05). Pretreatment of rats with TXR significantly reduced myocardial inflammatory cytokines TNF-α and IL-1β levels after I/R insult in diabetic as well as control hearts (P < 0.05). ConclusionPreconditioning with TXR could provide cardioprotection by anti-arrhythmic and anti-inflammatory effects against I/R injury in rat hearts. This effect of TXR can introduce this material as a protective agent in cardiovascular diseases.

Characteristics of the inferior wall hypertrophy in hypertrophic cardiomyopathy patients with contrast echocardiography

We tried to explore the value of contrast echocardiography (CEcho) on evaluating hypertrophic cardiomyopathy (HCM) with the inferior wall hypertrophy. A total of 114 patients with HCM were investigated. All the patients received CEcho and routine echocardiography (Echo), and 45 of them received cardiac magnetic resonance (CMR) and 47 of them received Holter. The frequency and percentage of inferior wall hypertrophy were analyzed in HCM patients, as well as the structure and function. The results showed that: (1) Inferior wall hypertrophy was detected in 55 patients (48%) by Echo, while 68 patients (60%) by CEcho. (2) There was no significant difference between CMR and CEcho in the measurement of inferior wall at end-diastole and end-systole. Thickness of inferior wall by CEcho tended to be higher than CMR. However, the inferior wall thickness measured by Echo was obviously lower than that by CMR ( P < 0.05) and CEcho ( P < 0.05). (3) Bland-Altman plot suggested good consistency between CEcho and CMR in measuring inferior wall thickness. 95% CI of mean differences in inferior wall thickness between CEcho and CMR were smaller in HCM patients as compared with that between Echo and CMR. Unary linear regression analysis showed good degree of fitting between CEcho and CMR. (4) Holter showed that HCM patients with inferior wall hypertrophy were likely to have higher incidence of premature ventricular complexes (PVC) ≥ 500/24 h. We demonstrate that CEcho is rather sensitive in detecting inferior wall hypertrophy. Echo may underestimate the inferior wall thickness. The risk of ventricular premature beats may increase in HCM patients with inferior hypertrophy.

Influence of vitamin D on the percentage time of cardiac resynchronization in patients with heart failure, premature ventricular complexes, and chronic kidney disease

IntroductionRecent studies have shown that in chronic kidney disease (CKD) 25(OH)D deficiency or insufficiency are a significant risk factor for cardiovascular diseases, sudden cardiac death and mortality. The high incidence of premature ventricular complexes (PVCs) have increasingly been recognized as a primary cause for worsening left ventricular systolic function and heart failure in some patients, specialty when these subjects are under optimal treatment and have implantable cardiac defibrillator (ICD) with cardiac resynchronization therapy (CRT), because the great amount of PVCs reduces the percentage of cardiac resynchronization. AimOur aim was to evaluate the influence of reposition of cholecalciferol in patients with deficiency of vitamin D in the changes of the numbers of PVCs, and consequently in the percentage of cardiac resynchronization time, during 6months of follow-up. Methods and resultsWe conducted a prospective, longitudinal study of 56 patients with high incidence of PVCs, heart failure under optimal treatment, ICD+CRT, deficiency of vitamin D (≤20ng/mL) and CKD (estimated glomerular filtration rate measured by MDRD equation, between 16 and 59mL/min/1.73m2). All patients were treated with cholecalciferol. We observed significant ameliorating after cholecalciferol onset in the number of PVCs, CRT % time, renal function, vitamin D levels and plasmatic ions at the 6th month of follow-up vs. baseline. ConclusionsWe suggest that the effectiveness of cholecalciferol reposition for subjects with high incidence of PVCs, heart failure under optimal treatment, ICD+CRT, deficiency of vitamin D and CKD, restoring the function of the CRT, bringing the biventricular pacing to nearby 97%.

Scn2b Deletion in Mice Results in Ventricular and Atrial Arrhythmias.

Mutations in SCN2B, encoding voltage-gated sodium channel β2-subunits, are associated with human cardiac arrhythmias, including atrial fibrillation and Brugada syndrome. Because of this, we propose that β2-subunits play critical roles in the establishment or maintenance of normal cardiac electric activity in vivo. To understand the pathophysiological roles of β2 in the heart, we investigated the cardiac phenotype of Scn2b null mice. We observed reduced sodium and potassium current densities in ventricular myocytes, as well as conduction slowing in the right ventricular outflow tract region. Functional reentry, resulting from the interplay between slowed conduction, prolonged repolarization, and increased incidence of premature ventricular complexes, was found to underlie the mechanism of spontaneous polymorphic ventricular tachycardia. Scn5a transcript levels were similar in Scn2b null and wild-type ventricles, as were levels of Nav1.5 protein, suggesting that similar to the previous work in neurons, the major function of β2-subunits in the ventricle is to chaperone voltage-gated sodium channel α-subunits to the plasma membrane. Interestingly, Scn2b deletion resulted in region-specific effects in the heart. Scn2b null atria had normal levels of sodium current density compared with wild type. Scn2b null hearts were more susceptible to atrial fibrillation, had increased levels of fibrosis, and higher repolarization dispersion than wild-type littermates. Genetic deletion of Scn2b in mice results in ventricular and atrial arrhythmias, consistent with reported SCN2B mutations in human patients.

Gap junction modifier rotigaptide decreases the susceptibility to ventricular arrhythmia by enhancing conduction velocity and suppressing discordant alternans during therapeutic hypothermia in isolated rabbit hearts

Therapeutic hypothermia (TH) may increase the susceptibility to ventricular arrhythmias by decreasing ventricular conduction velocity (CV) and facilitating arrhythmogenic spatially discordant alternans (SDA). The purpose of this study was to test the hypothesis that rotigaptide, a gap junction enhancer, can increase ventricular CV, delay the onset of SDA, and decrease the susceptibility to pacing-induced ventricular fibrillation (PIVF) during TH. Langendorff-perfused isolated rabbit hearts were subjected to 30-minute moderate hypothermia (33°C) followed by 20-minute treatment with rotigaptide (300 nM, n = 8) or vehicle (n = 5). The same protocol was also performed at severe hypothermia (30°C; n = 8 for rotigaptide, n = 5 for vehicle). Using an optical mapping system, epicardial CV and SDA threshold were evaluated by S1 pacing. Ventricular fibrillation inducibility was evaluated by burst pacing for 30 seconds at the shortest pacing cycle length (PCL) that achieved 1:1 ventricular capture. Rotigaptide increased ventricular CV during 33°C (PCL 300 ms, from 76 ± 6 cm/s to 84 ± 7 cm/s, P = .039) and 30°C (PCL 300 ms, from 62 ± 6 cm/s to 68 ± 4 cm/s, P = .008). Rotigaptide decreased action potential duration dispersion at 33°C (P = .01) and 30°C (P = .035). During 30°C, SDA thresholds (P = .042) and incidence of premature ventricular complexes (P = .025) were decreased by rotigaptide. PIVF inducibility was decreased by rotigaptide at 33°C (P = .039) and 30°C (P = .042). Rotigaptide did not change connexin43 expressions and distributions during hypothermia. Rotigaptide protects the hearts against ventricular arrhythmias by increasing ventricular CV, delaying the onset of SDA, and reducing repolarization heterogeneity during TH. Enhancing cell-to-cell coupling by rotigaptide might be a novel approach to prevent ventricular arrhythmias during TH.

Anesthetic complications due to extremely low ankle blood pressure caused by peripheral arterial disease

Anesthetic complications due to extremely low ankle blood pressure caused by peripheral arterial disease

Cytosolic calcium accumulation and delayed repolarization associated with ventricular arrhythmias in a guinea pig model of Andersen-Tawil syndrome

Andersen-Tawil syndrome (ATS1)-associated ventricular arrhythmias are initiated by frequent, hypokalemia-exacerbated, triggered activity. Previous ex vivo studies in drug-induced Andersen-Tawil syndrome (DI-ATS1) models have proposed that arrhythmia propensity in DI-ATS1 derives from cytosolic Ca(2+) ([Ca(2+)](i)) accumulation leading to increased triggered activity. The purpose of this study was to test the hypothesis that elevated [Ca(2+)](i) with concomitant APD prolongation, rather than APD dispersion, underlies arrhythmia propensity during DI-ATS1. DI-ATS1 was induced in isolated guinea pig ventricles by perfusion of 2 mM KCl Tyrode solution containing 10 μM BaCl(2). APD and [Ca(2+)](i) from the anterior epicardium were quantified by ratiometric optical voltage (di-4-ANEPPS) or Ca(2+) (Indo-1) mapping during right ventricular pacing with or without the ATP-sensitive potassium channel opener pinacidil (15 μM). APD gradients under all conditions were insufficient for arrhythmia induction by programmed stimulation. However, 38% of DI-ATS1 preparations experienced ventricular tachycardias (VTs), and all preparations experienced a high incidence of premature ventricular complexes (PVCs). Pinacidil decreased APD and APD dispersion and reduced VTs (to 6%), and PVC frequency (by 79.5%). However, PVC frequency remained significantly greater relative to control (0.5% ± 0.3% of DI-ATS1). Importantly, increased arrhythmia propensity during DI-ATS1 was associated with diastolic [Ca(2+)](i) accumulation and increased [Ca(2+)](i) transient amplitudes. Pinacidil partially attenuated the former but did not alter the latter. The study data suggest that arrhythmias during DI-ATS1 may be a result of triggered activity secondary to prolonged APD and altered [Ca(2+)](i) cycling and less likely dependent on large epicardial APD gradients forming the substrate for reentry. Therefore, therapies aimed at reducing [Ca(2+)](i) rather than APD gradients may prove effective in treatment of ATS1.

The p75 neurotrophin receptor, semaphorins, and sympathetic traffic in the heart

the sympathetic and parasympathetic branches of the autonomic nervous system control cardiac function through the coordinated activity generated by neurons within the intracardiac autonomic ganglia and central nervous system (3). Activation of the sympathetic efferent projections to the heart increases heart rate, modifies the pattern and conduction velocity of the impulse through the heart, and augments both atrial and ventricular contractility while hastening myocardial relaxation. In the vasculature, the sympathetic nervous system (SNS) reduces venous capacitance and constricts resistance vessels, increasing blood pressure. Conversely, the parasympathetic nervous system (PSNS) decreases heart rate and cardiac impulse conduction. More recent evidence has suggested that the PSNS may also affect ventricular function, indirectly by countering β-adrenergic action or directly via inhibition of L-type Ca2+ channels (34). A transient imbalance between these two branches can lead to increased heart rate and blood pressure when cardiac output is increased. When subnormal cardiac PSNS activity concomitant with sympathetic hyperactivation persists, such as after myocardial infarction, this disequilibrium may increase the risk for cardiac adverse events, including arrhythmias, hypertension, cardiac hypertrophy, and, ultimately, heart failure. This condition is called “autonomic neural remodeling” and can greatly contribute to the induction of ventricular fibrillation, thus increasing the patient's susceptibility to sudden cardiac death (41, 47). It is plausible that neurotrophic factors, target organ-secreted proteins essential for the development and differentiation of neurons, are involved in the remarkable neuroplasticity exhibited by the SNS in the adult life, including autonomic remodeling after infarction and/or in the onset and progression of congestive heart failure (17, 30, 32).

Safety and Feasibility of Real Time Adenosine Myocardial Contrast Echocardiography with Emphasis on Induction of Arrhythmias: A Study in Healthy Volunteers and Patients with Stable Coronary Artery Disease

Some studies reported an increased incidence of premature ventricular complexes (PVCs) during triggered myocardial contrast echocardiography (MCE) using high-intensity ultrasound destruction. Whether PVCs are also induced by real time MCE using low emission power, is unknown. The aim of the study was to assess the occurrence of arrhythmias during real time adenosine MCE in healthy volunteers and patients with stable coronary artery disease (CAD). Fifty healthy volunteers and 26 patients with stable CAD underwent real time MCE using Sonovue and power pulse inversion (ATL 5000) at rest and during adenosine stress. The occurrence of premature atrial complexes (PAC) and PVCs was analyzed before and during MCE using ECG-tracings from videotapes. In healthy subjects, the occurrence of PVCs at baseline (0.04 +/- 0.23 PVCs/min) was similar at rest (0.04 +/- 0.23 PVCs/min, P = NS), and adenosine stress (0.03 +/- 0.14, P = NS). In CAD patients, the occurrence of PVCs at baseline was 0.30 +/- 0.76 PVC/min, compared to 0.29 +/- 0.74 at rest (P = NS), and 0.34 +/- 0.74 during adenosine stress (P = NS). The number of subjects demonstrating PVCs did not increase during MCE. The occurrence of PACs during MCE was not increased compared to baseline. Real time MCE using low emission power does not increase the occurrence of premature complexes in healthy volunteers or CAD patients.

Absence of gp130 in dopamine β-hydroxylase-expressing neurons leads to autonomic imbalance and increased reperfusion arrhythmias

Inflammatory cytokines that act through glycoprotein (gp)130 are elevated in the heart after myocardial infarction and in heart failure. These cytokines are potent regulators of neurotransmitter and neuropeptide production in sympathetic neurons but are also important for the survival of cardiac myocytes after damage to the heart. To examine the effect of gp130 cytokines on cardiac nerves, we used gp130(DBH-Cre/lox) mice, which have a selective deletion of the gp130 cytokine receptor in neurons expressing dopamine beta-hydroxylase (DBH). Basal sympathetic parameters, including norepinephrine (NE) content, tyrosine hydroxylase expression, NE transporter expression, and sympathetic innervation density, appeared normal in gp130(DBH-Cre/lox) compared with wild-type mice. Likewise, basal cardiovascular parameters measured under isoflurane anesthesia were similar in both genotypes, including mean arterial pressure, left ventricular peak systolic pressure, dP/dt(max), and dP/dt(min). However, pharmacological interventions revealed an autonomic imbalance in gp130(DBH-Cre/lox) mice that was correlated with an increased incidence of premature ventricular complexes after reperfusion. Stimulation of NE release with tyramine and infusion of the beta-agonist dobutamine revealed blunted adrenergic transmission that correlated with decreased beta-receptor expression in gp130(DBH-Cre/lox) hearts. Due to the developmental expression of the DBH-Cre transgene in parasympathetic ganglia, gp130 was eliminated. Cholinergic transmission was impaired in gp130(DBH-Cre/lox) hearts due to decreased parasympathetic drive, but tyrosine hydroxylase immunohistochemistry in the brain stem revealed that catecholaminergic nuclei appeared grossly normal. Thus, the apparently normal basal parameters in gp130(DBH-Cre/lox) mice mask an autonomic imbalance that includes alterations in sympathetic and parasympathetic transmission.

Ventricular arrhythmias and changes in heart rate preceding ventricular tachycardia in patients with an implantable cardioverter defibrillator

The objective was to determine the characteristics of heart rate variability and ventricular arrhythmias prior to the onset of ventricular tachycardia (VT) in patients with an implantable cardioverter defibrillator (ICD). Sixty-eight beat-to-beat time series from 13 patients with an ICD were analyzed to quantify heart rate variability and ventricular arrhythmias. The episodes of VT were classified in one of two groups depending on whether the sinus rate in the 1 min preceding the VT was greater or less than 90 beats per minute. In a subset of patients, increased heart rate and reduced heart rate variability was often observed up to 20 min prior to the VT. There was a non-significant trend to higher incidence of premature ventricular complexes (PVCs) before VT compared to control recordings. The patterns of the ventricular arrhythmias were highly heterogeneous among different patients and even within the same patient. Analysis of the changes of heart rate and heart rate variability may have predictive value about the onset of VT in selected patients. The patterns of ventricular arrhythmia could not be used to predict onset of VT in this group of patients.

Effect of acute hypertension on the cardiac rhythm. Experimental observations

An acute increase in blood pressure (BP) may be associated with the genesis of ventricular ectopy. Fourteen anesthetized dogs were examined to find out whether the critical pressure that causes an arrhythmia may be an index of the tendency of the myocardium to generate ectopic rhythms. An acute change in BP was produced 321 times using an arterial pressure reservoir or aortic obstruction or a metaraminol infusion or, inversely, arterial bleeding. Each time the BP was increased, cardiac arrhythmias appeared and each time the BP was decreased the cardiac arrhythmias disappeared. The most common type of arrhythmia was ventricular ectopy (123/167 acute BP increases), usually in a form of bigeminy. The next most common rhythm disturbance was atrioventricular block (32/167 acute BP increases), especially when a constant rate was achieved by atrial pacing. The BP above which an arrhythmia appeared varied greatly among different animals (189.0 +/- 55.1 mmHg, means +/- SD). It was significantly (p less than 0.01) reduced (-29.0 +/- 17.1 mmHg) following coronary ligation and significantly (p less than 0.05) raised (+/- 41.6 +/- 38.7 mmHg) following lidocaine administration. The incidence of ventricular ectopy on increasing the BP was significantly higher at low heart rates in ten experiments, lower in two and not significantly different in 14. The incidence of premature ventricular complexes, the degree of atrioventricular block and the PR interval in first-degree atrioventricular block, whenever these rhythm disorders appeared, were a function of the BP level. It is concluded that an acute increase in BP may cause rhythm disturbances, usually in the form of ventricular ectopy and/or atrioventricular block.(ABSTRACT TRUNCATED AT 250 WORDS)

Characteristics of the action of Crotalus horridus horridus (timber rattlesnake) venom on the isolated, perfused rat heart

R. Kempsford and B. J. Hawgood. Characteristics of the action of Crotalus horridus horridus (timber rattlesnake) venom on the isolated, perfused rat heart. Toxicon 25, 1311 – 1319, 1987. — The isolated Langendorff-perfused heart was used to examine the effects of a 4 min infusion of Crotalus horridus horridus venom (3.3 – 33 μg/ml) on various physiological, biochemical and morphological parameters. Venom infusion reduced ventricular contractility in a dose-dependent manner that was not reversible; this response was markedly attenuated by either lowering the temperature from 37°C to 32°C or the perfusate potassium ion concentration from 5.9 to 2.5 mM. The negative inotropic response was not associated with any change in heart rate or coronary flow. Envenomation induced a progressive fall in ECG amplitude without effect on P and Q waves and a variable delayed incidence of premature ventricular complexes. Light microscopy showed localized, patchy areas of degenerating fibres within the ventricular mass by 5 min. Ventricular tissue ATP, ADP and lactate content were not significantly changed at this time. Crotamine was without effect on the heart. Another venom component apparently has a direct effect on the heart to disrupt the integrity of ventricular fibres.

Acute changes in blood pressure as a cause of cardiac arrhythmias.

The effect of an acute change in blood pressure (BP) on ventricular ectopic activity and the influence of antiarrhythmic agents on this effect were examined in 24 patients. In 11 patients with premature ventricular complexes (PVCs), the BP was temporarily reduced by a sodium nitroprusside drip. In all of them the incidence of PVCs was reduced (or annihilated) by the induced hypotension. In 13 patients without ventricular ectopic activity, a metaraminol drip was given until either a PVC appeared or the systolic BP reached 200 mmHg, or symptoms appeared. In 12 cases at least one PVC appeared and in 8 of them the total number of PVCs was 13 or more, usually in the form of bigeminy. The repetition of the test following quinidine administration (serum quinidine level 1.7 +/- 0.5 ng ml-1) in 6 cases did not change this pattern, with one exception. It prevented the appearance of idioventricular accelerated rhythm in one case in whom this rhythm had been induced by the hypertension provocative test before the quinidine administration. All cases, in whom the test failed to induce more than 3 PVCs, had no cardiac problem at all. Six of the 8 cases in whom the test induced 13 or more PVCs had organic cardiac disease or palpitation. Other arrhythmias observed on BP elevation, were supraventricular extra beats, nodal escape rhythms and atrioventricular block. In one case with cardiomyopathy, the BP elevation was associated with early signs of heart failure that subsided quickly. In conclusion, acute elevation on BP may be associated with the generation of PVCs and its reduction with their reduction or disappearance.

Cardiac arrhythmias in end-stage renal disease.

In 16 patients with end-stage renal disease (ESRD), 24-hour electrocardiographic recordings showed an incidence of supraventricular and ventricular arrhythmias similar to that in patients who had had myocardial infarction and in low-risk subjects. Eight patients (50%) with ESRD had supraventricular complexes. This incidence was significantly higher than that after myocardial infarction (P < .001). Fifteen ESRD patients (94%) had premature ventricular complexes (PVCs), including nine (56%) with complex PVCs (multiform PVCs, couplets, or runs). The incidence of PVCs as well as complex PVCs in patients with ESRD was comparable to that of the patients who had had myocardial infarction but was significantly higher than that found in low-risk subjects (P less than .005 for PVCs and P less than .05 for complex PVCs). The high incidence of complex PVCs in patients with ESRD may predispose them to increased cardiovascular death, and further investigation of this finding is indicated.

Nitroglycerin and premature ventricular complexes in myocardial infarction.

Because of clinical observations suggesting that nitroglycerin may suppress premature ventricular complexes during acute ischaemia, a study was undertaken to assess the effect of nitroglycerin on the incidence of premature ventricular complexes in patients with acute myocardial infarction. Forty patients with acute myocardial infarction were studied. Twenty-six patients received 0.4 mg nitroglycerin sublingually every 4 hours for the first 24 hours after admission to the coronary care unit. The total premature ventricular complex count for the 26 patients for 15 minutes before nitroglycerin was 592, and 276 for the 15 minutes after the drug (P less than 0.005). In the remaining 14 patients on the same nitroglycerin schedule, a single electrocardiographic lead was continuously recorded on tape. During the first hour after nitroglycerin, the premature ventricular complex count decreased by 58 per cent, and the second and third hours showed a decrease from control count of 71 and 65 per cent respectively. By the end of 4 hours the ectopic count was back to control level. The data indicate that nitroglycerin may decrease the number of premature ventricular complexes for up to 3 hours in patients with acute myocardial infarction. The mechanism of action of nitroglycerin is not elucidated by this study, but the observation may be of value in further studies of specific antiarrhythmic therapy and prevention of arrhythmias in patients with coronary artery disease.