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Biomedical subjects

G A Haywood

Publications and source records attributed to G A Haywood.

At least 19 recordsLinked to original sources
PubMed2005

Disease progression and adverse events in patients listed for elective percutaneous coronary intervention.

OBJECTIVE: To record disease progression and the timing of adverse events in patients on a waiting list for elective percutaneous coronary intervention (PCI). DESIGN: Observational prospective study. SETTINGS: A UK tertiary cardiothoracic centre, at a time when waiting lists for PCI were up to 18 months. PATIENTS: 145 patients (116 men, median age 59.5 years) placed on an elective waiting list for PCI between October 1998 and September 1999. MAIN OUTCOME MEASURES: Adverse events recorded were death, myocardial infarction, need for urgent hospital admission because of unstable angina, and need for emergency revascularisation while waiting for PCI. RESULTS: During a median follow up of 10 months (range 1-18 months), nine (6.2%) patients experienced an adverse event. Eight (5.52%) patients were admitted with unstable angina as emergencies. One was admitted with a myocardial infarction. Twenty nine (20.0%) patients had significant disease progression at the time of the repeat angiogram before PCI. In 10 (7%), disease had progressed so that PCI was no longer feasible and patients were referred for coronary artery bypass graft. Sixteen (11%) were removed from the PCI waiting list because of almost complete resolution of their anginal symptoms. CONCLUSION: Adverse coronary events and clinically significant disease progression occur commonly in patients waiting for PCI. Despite the presence of severe coronary lesions, myocardial infarction was rare and no patients died while on the waiting list. Resolution of anginal symptoms was also comparatively common. The pathophysiology of disease progression frequently necessitates a change in the treatment of patients waiting for PCI.

Adult↗
PubMed2001

Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay.

BACKGROUND: One third of patients with chronic heart failure have electrocardiographic evidence of a major intraventricular conduction delay, which may worsen left ventricular systolic dysfunction through asynchronous ventricular contraction. Uncontrolled studies suggest that multisite biventricular pacing improves hemodynamics and well-being by reducing ventricular asynchrony. We assessed the clinical efficacy and safety of this new therapy. METHODS: Sixty-seven patients with severe heart failure (New York Heart Association class III) due to chronic left ventricular systolic dysfunction, with normal sinus rhythm and a duration of the QRS interval of more than 150 msec, received transvenous atriobiventricular pacemakers (with leads in one atrium and each ventricle). This single-blind, randomized, controlled crossover study compared the responses of the patients during two periods: a three-month period of inactive pacing (ventricular inhibited pacing at a basic rate of 40 bpm) and a three-month period of active (atriobiventricular) pacing. The primary end point was the distance walked in six minutes; the secondary end points were the quality of life as measured by questionnaire, peak oxygen consumption, hospitalizations related to heart failure, the patients' treatment preference (active vs. inactive pacing), and the mortality rate. RESULTS: Nine patients were withdrawn from the study before randomization, and 10 failed to complete both study periods. Thus, 48 patients completed both phases of the study. The mean distance walked in six minutes was 22 percent greater with active pacing (399+/-100 m vs. 326+/-134 m, P<0.001), the quality-of-life score improved by 32 percent (P<0.001), peak oxygen uptake increased by 8 percent (P<0.03), hospitalizations were decreased by two thirds (P<0.05), and active pacing was preferred by 85 percent of the patients (P<0.001). CONCLUSIONS: Although it is technically complex, atriobiventricular pacing significantly improves exercise tolerance and quality of life in patients with chronic heart failure and intraventricular conduction delay.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Intracoronary Multi-link stents: experience in 218 patients using aspirin alone.

OBJECTIVES: To assess procedural outcome, complications, and clinical follow up in 218 patients who underwent treatment with 297 Multi-link (Guidant) stents implanted without the use of intravascular ultrasound (IVUS) or quantitative coronary angiography (QCA), and using aspirin alone as antiplatelet therapy. METHODS: The case records and angiograms were reviewed and the patients were contacted by telephone to determine their symptoms and any adverse events at follow up. Data were analysed using Fisher's exact test. RESULTS: Of the 218 patients included in the study, 45 had multivessel intracoronary intervention, and 55 had unstable angina. The mean (SD) length of hospital stay following the procedure was 2.0 (2.1) days. There were two early deaths at less than 30 days, and two deaths during follow up at more than 100 days. Ten patients suffered complications during the first 30 days: four had subacute stent thrombosis, of whom two died and two were treated successfully with coronary artery bypass grafting; five had a non-Q wave myocardial infarction; and one had a femoral false aneurysm. Patient outcome was analysed according to stent diameter (3.0 mm or less, or 3.5 mm or more) and by angina status (stable or unstable). In patients in whom at least one stent was 3.0 mm diameter, four of 86 patients suffered acute stent occlusion, whereas in the 132 patients in whom all stents were at least 3.5 mm diameter there were no cases of stent occlusion (p = 0.02). In the unstable angina group two of 55 patients suffered acute stent occlusion compared to two of 163 patients in the stable angina group (NS). In patients with unstable angina and at least one stent of 3.0 mm diameter, the acute occlusion rate was 7.1% (two of 28 patients). Three of the four patients with stent occlusion had undergone complex procedures. Twenty eight patients were restudied for recurrent symptoms during the follow up period. Of these, eight patients had restenosis within their stent. In seven of these patients the stent size was 3.0 mm diameter, and in the remaining patient the stent size was 4.0 mm diameter. Three of the 28 patients restudied had developed new disease remote from the stented site, and 17 had patent stents and no significant other coronary lesion. CONCLUSIONS: This study suggests that coronary intervention using the Multi-link stent is safe and effective using aspirin alone, without IVUS or QCA, when stent diameter is greater than 3.0 mm. All cases of stent occlusion in this series occurred in patients in whom at least one stent was 3.0 mm diameter, with stent occlusion being higher in patients with unstable angina compared to those with stable angina. Additional antiplatelet therapy may be beneficial in those patients in whom Multi-link stent diameter is less than 3.5 mm, particularly in those with unstable angina, but is not necessary for patients receiving Multi-link stents of 3.5 mm diameter or greater.

Adult↗
PubMed1997

AT1 and AT2 angiotensin receptor gene expression in human heart failure.

BACKGROUND: The availability of selective antagonists for angiotensin II receptors has focused interest on the gene expression of angiotensin II-receptor subtypes in the human heart. METHODS AND RESULTS: We analyzed expression of the AT1 and AT2 subtypes of the angiotensin II receptor in ventricular myocardium taken from 9 donor hearts before implantation and from 12 patients with heart failure (6 with dilated cardiomyopathy and 6 with ischemic heart disease). Competitive reverse transcription-polymerase chain reaction with synthetic RNA internal standards was used to detect mRNA for both subtypes and to quantify relative differences in levels between failing and non-failing ventricular myocardium. AT1- and AT2-receptor mRNA could be detected in all samples. AT1-receptor gene expression was 2.5-fold greater in nonfailing hearts than in patients with failing hearts (P = .015). There was no significant difference in AT2-receptor mRNA expression in failing and nonfailing hearts. CONCLUSIONS: The level of expression of the angiotensin AT1 receptor appears to decrease in the failing human ventricle whereas the level of AT2 expression is unaffected. These changes parallel the changes found in human ventricular myocardium at the receptor level, suggesting that the changes in receptor level may result from changes in gene expression or mRNA stability.

Adult↗
PubMed1996

Expression of inducible nitric oxide synthase in human heart failure.

BACKGROUND: There is increasing evidence that alterations in nitric oxide synthesis are of pathophysiological importance in heart failure. A number of studies have shown altered nitric oxide production by the endothelial constitutive isoform of nitric oxide synthase (NOS), but there is very little information on the role of the inducible isoform. METHODS AND RESULTS: We analyzed inducible NOS (iNOS) expression in ventricular myocardium taken from 11 control subjects (who had died suddenly from noncardiac causes), from 10 donor hearts before implantation, and from 51 patients with heart failure (24 with dilated cardiomyopathy [DCM], 17 with ischemic heart disease [IHD], and 10 with valvular heart disease [VHD]). Reverse transcription-polymerase chain reaction was used to confirm the presence of intact mRNA and to detect expression of iNOS and atrial natriuretic peptide (ANP). ANP was used as a molecular phenotypic marker of ventricular failure. iNOS was expressed in 36 of 51 biopsies (71%) from patients with heart failure and in none of the control patients (P<.0001). iNOS expression could also be detected in 50% of the donor hearts. All samples that expressed iNOS also expressed ANP. iNOS gene expression occurred in 67% of patients with DCM, 59% of patients with IHD, and 100% of patients with VHD. To determine whether iNOS protein was expressed in failing ventricles, immunohistochemistry was performed on three donor hearts and nine failing hearts with iNOS mRNA expression. Staining for iNOS was almost undetectable in the donor myocardium and in control sections, but all failing hearts showed diffuse cytoplasmic staining in cardiac myocytes. Expression of iNOS could be observed in all four chambers. Western blot analysis with the same primary antibody showed a specific positive band for iNOS protein in the heart failure specimens; minimal iNOS protein expression was seen in donor heart samples. CONCLUSIONS: iNOS expression occurs in failing human cardiac myocytes and may be involved in the pathophysiology of DCM, IHD, and VHD.

Adult↗
PubMed1996

Induction of nitric oxide synthase in the human cardiac allograft is associated with contractile dysfunction of the left ventricle.

BACKGROUND: The mechanisms underlying cardiac contractile dysfunction after transplantation remain poorly defined. Previous work has revealed that inducible nitric oxide synthase (iNOS) is expressed in the rat heterotopic cardiac allograft during rejection; resultant overproduction of nitric oxide (NO) might cause cardiac contractile dysfunction via the negative inotropic and cytotoxic actions of NO. In this investigation, we tested the hypothesis that induction of iNOS may occur and be associated with cardiac allograft contractile dysfunction in humans. METHODS AND RESULTS: We prospectively studied 16 patients in the first year after cardiac transplantation at the time of serial surveillance endomyocardial biopsy. Clinical data, the results of biopsy histology, and echocardiographic and Doppler evaluation of left ventricular systolic and diastolic function were recorded. Total RNA was extracted from biopsy specimens, and mRNA for beta-actin, detected by reverse transcription-polymerase chain reaction (RT-PCR) using human specific primers, was used as a constitutive gene control; iNOS mRNA was similarly detected by RT-PCR using human specific primers. iNOS protein was detected in biopsy frozen sections by immunofluorescence. Myocardial cGMP was measured by radioimmunoassay, and serum nitrogen oxide levels (NOx = NO2 + NO3) were measured by chemiluminescence. iNOS mRNA was detected in allograft myocardium at some point in each patient and in 59 of 123 biopsies (48%) overall. In individual patients, iNOS mRNA expression was episodic and time dependent; the frequency of expression was highest during the first 180 days after transplant (P = .0006). iNOS protein associated with iNOS mRNA was detected by immunofluorescence in cardiac myocytes. iNOS mRNA expression was not related to the ISHLT histological grade of rejection or to serum levels of NOx but was associated with increased levels of myocardial cGMP (P = .01) and with both systolic (P = .024) and diastolic (P = .006) left ventricular contractile dysfunction measured by echocardiography and Doppler. CONCLUSIONS: These data support a relation between iNOS mRNA expression and contractile dysfunction in the human cardiac allograft.

Adolescent↗
PubMed1996

Transplant candidates with severe left ventricular dysfunction managed with medical treatment: characteristics and survival.

OBJECTIVES: This study sought to assess the clinical characteristics and survival of patients with symptomatic heart failure who were referred as potential heart transplant candidates, but were selected for medical management. BACKGROUND: Patients with severe left ventricular dysfunction referred for heart transplantation may be considered too well to be placed immediately on an active waiting transplant list. The clinical characteristics of this patient group and their survival have not been well defined. These patients represent a unique group that are characterized by comparatively low age and freedom from significant comorbid conditions. METHODS: We studied 116 consecutive patients with symptomatic heart failure, severe left ventricular dysfunction (left ventricular ejection fraction 20 +/- 7% [mean +/- SD]) and duration of symptoms >1 month referred for heart transplantation, who were acceptable candidates for the procedure but who were not listed for transplantation because of relative clinical stability. These patients were followed up closely on optimal medical therapy. A variety of baseline clinical, hemodynamic and exercise variables were assessed to define this patient group and used to predict cardiac death and requirement later for heart transplantation. RESULTS: During a mean follow-up period of 25.0 +/- 14.8 months (follow-up 99% complete), there were eight cardiac deaths (7%) (seven sudden, one acute myocardial infarction). Only nine patients (8%) were listed for heart transplantation. Actuarial 1- and 4-year cardiac survival rates were 98 +/- 1% and 84 +/- 7% (mean +/- SE), respectively, and freedom from listing for transplantation was 95 +/- 2% and 84 +/- 7% (mean +/- SE), respectively. Patients were mainly in New York Heart Association functional class II or III and had a preserved cardiac index (2.4 liters/min.m2), pulmonary capillary wedge pressure of 16 +/- 9 mm Hg (mean +/- SD) and maximal oxygen consumption of 17.4 +/- 4.3 ml/min per kg (mean +/- SD). By logistic regression analysis, there was no predictor for cardiac death. Longer duration of heart failure (p = 0.013) and mean pulmonary artery (p < 0.05) and pulmonary systolic (p = 0.014) and diastolic (p < 0.05) pressures correlated significantly with listing for heart transplantation by univariate logistic regression. By multivariate logistic regression, only pulmonary artery systolic pressure (p < 0.004) and duration of heart failure (p < 0.015) remained as predictors for need for later transplantation. CONCLUSIONS: In the current treatment era, prognosis is favorable in a definable group of transplant candidates despite severe left ventricular dysfunction. This patient group can be identified after intensive medical therapy by stable symptoms, a relatively high maximal oxygen uptake at peak exercise and a preserved cardiac output.

Adult↗
PubMed1996

Analysis of deaths in patients awaiting heart transplantation: impact on patient selection criteria.

OBJECTIVE: To analyse the clinical characteristics of patients who died on the Stanford heart transplant waiting list and to develop a method for risk stratifying status 2 patients (outpatients). METHODS: Data were reviewed from all patients over 18 years, excluding retransplants, who were accepted for heart transplantation over an eight year period from 1986 to 1994. RESULTS: 548 patients were accepted for heart transplantation; 53 died on the waiting list, and 52 survived on the waiting list for over one year. On multivariate analysis only peak oxygen consumption (peak VO2: 11.7 (SD 2.7) v 15.1 (5.2) ml/kg/min, P = 0.02) and cardiac output (3.97 (1.03) v 4.79 (1.06) litres/min, P = 0.04) were found to be independent prognostic risk factors. Peak VO2 and cardiac index (CI) were then analysed in the last 141 consecutive patients accepted for cardiac transplantation. All deaths and 88% of the deteriorations to status 1 on the waiting list occurred in patients with either a CI < 2.0 or a VO2 < 12. In those with a CI < 2.0 and a VO2 < 12, 38% died or deteriorated to status 1 in the first year on the waiting list. Patients with CI > or = 2.0 and a VO2 > or = 12 all survived throughout follow up. Using a Cox's proportional hazards model with CI and peak VO2 as covariates, tables were constructed predicting the chance of surviving for (a) 60 days and (b) 1 year on the waiting list. CONCLUSIONS: These data provide a basis for risk stratification of status 2 patients on the heart transplant waiting list.

Cardiac Output↗
PubMed1995

Is there a role for epoprostenol in the management of heart failure?

Prostacyclin (PGI2, epoprostenol), a pulmonary and systemic vasodilating agent, has recently undergone long-term intravenous administration trials in patients with severe congestive heart failure. As in many other agents that have beneficial acute hemodynamic profiles, its effects on mortality have been disappointing. However, the drug continues to have a role in the short-term management of patients with decompensated heart failure because of its short half-life, lack of medium-term toxicity compared to sodium nitroprusside, and lesser tendency toward development of tolerance than intravenous nitrates. There may also be therapeutic effects other than its influence on central hemodynamics; in particular, inhibition of platelet aggregation and thrombus formation in small vessels may be of value in the long-term management of patients with primary pulmonary hypertension. It is possible that, like other agents such as vesnarinone (OPC-8212), achieving beneficial long-term effects may require identification of an ideal dose range. The most effective therapeutic doses in long-term administration may not correlate with the most effective doses during short-term hemodynamic studies.

Epoprostenol↗
PubMed1995

Short-term effects of intra-aortic balloon pumping on renal blood flow and renal oxygen consumption in cardiogenic shock.

Intra-aortic balloon pumping is frequently used in patients with cardiogenic shock when oliguria persists despite maximal pharmacologic support. The objective of this study was to measure the effect of intra-aortic balloon pumping on renal blood flow, renal oxygen delivery, and renal oxygen consumption in such patients. Central hemodynamics, renal blood flow, and oxygen transport were measured in 10 patients in low cardiac output states. Measurements were made with and without intra-aortic balloon counterpulsation. Renal blood flow was measured by continuous renal vein thermodilution. Small improvements were observed in cardiac output (3.1 +/- 0.8 vs 3.5 +/- 0.8 L/min, P < .01) and pulmonary capillary wedge pressure (22 +/- 5.6 vs 19 +/- 5.3 mmHg, P < .05), but mean arterial blood pressure was unchanged (69 +/- 11 vs 69 +/- 5 mmHg, not significant). Baseline renal blood flow was reduced to approximately 37%, renal oxygen delivery to 31%, and renal oxygen consumption to 60% of normal values. No significant improvement was seen in single-kidney renal blood flow (184 +/- 108 vs 193 +/- 107 mL/min), renal oxygen delivery (28 +/- 16 vs 30 +/- 16 mL/min), or renal oxygen consumption (4.9 +/- 2.0 vs 4.7 +/- 2.5 mL/min) in response to 1:1 counterpulsation. In comparison with measurements made during short-term suspension of counterpulsation, 1:1 aortic balloon pumping failed to result in an increase in renal blood flow, oxygen delivery, or oxygen consumption from the low levels observed in these patients.

Adult↗
PubMed1993

Effects of long-term oral magnesium chloride replacement in congestive heart failure secondary to coronary artery disease.

Magnesium deficiency frequently develops in patients with congestive heart failure and may increase susceptibility to lethal arrhythmias and sudden death via multiple pathophysiologic mechanisms. The effects of peroral magnesium supplementation were investigated in a randomized, double-blind, crossover trial involving 21 patients with stable congestive heart failure secondary to coronary artery disease. All were receiving long-term loop diuretics, and had normal renal function, and low or normal serum magnesium concentrations. Subjects alternately received enteric-coated magnesium chloride (15.8 mmol magnesium per day) and placebo for 6 weeks. Magnesium therapy increased serum magnesium from 0.87 +/- 0.07 to 0.92 +/- 0.05 mmol/liter (p < 0.05), serum potassium from 4.0 +/- 0.3 to 4.3 +/- 0.4 mmol/liter (p < 0.01) and urinary magnesium excretion from 2.82 +/- 0.96 to 4.74 +/- 2.38 mmol/24 hours (p = 0.001). There was no significant change in heart rate or Doppler cardiac index, but mean arterial pressure decreased from 91 +/- 10 to 87 +/- 10 mm Hg (p < 0.05) and systemic vascular resistance from 1,698 +/- 367 to 1,613 +/- 331 dynes s cm-5 (p = 0.047). The frequency of isolated ventricular premature complexes was reduced by 23% (95% confidence interval [CI] 6 to 37%; p < 0.02), couplets by 52% (95% CI 30 to 65%; p < 0.001) and nonsustained ventricular tachycardia episodes by 24% (95% CI 15 to 49%; p < 0.01). Plasma epinephrine decreased from 447 +/- 535 to 184 +/- 106 pg/ml (p = 0.02), but there was no corresponding change in plasma norepinephrine or heart rate variability.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1993

Impaired immediate vasoconstrictor responses in patients with recurrent neurally mediated syncope.

Immediate responses to head-up tilt were determined in 78 consecutive patients with unexplained syncope undergoing 45-minute tilt tests at 60 degrees. Thirty-four patients developed neurally mediated syncope (mean time to syncope 18 minutes), 40 tolerated the full duration of tilt, and 4 were unable to complete the study but did not develop syncope. Blood pressure, heart rate, forearm blood flow and forearm vascular resistance were measured at baseline and after 2 and 5 minutes of tilt. Syncopal and nonsyncopal patients were well-matched for age and baseline hemodynamic parameters. There was no difference between the groups in heart rate or blood pressure at 2 minutes, but there was a small but significant difference in percent reduction in mean arterial pressure at 5 minutes. After 2 and 5 minutes of tilt, mean forearm blood flow was 2.4 and 2.6 ml/min/100 ml, respectively, in syncopal patients compared with 1.6 (p < 0.05) and 1.7 ml/min/100 ml (p < 0.01), respectively, in patients who tolerated 45 minutes of tilt. In syncopal patients, forearm vascular resistance was 51.0 and 44.0 at 2 and 5 minutes, respectively, whereas in nonsyncopal patients, it was 82.4 (p < 0.02) and 73.1 (p < 0.001), respectively. These differences remained consistent when only data for patients developing syncope after > 15 minutes were included in the analysis. Patients with neurally mediated syncope have clearly demonstrable abnormalities in vascular control immediately after assumption of the upright posture. The results shed new light on the pathophysiology of neurally mediated syncope.

Adolescent↗
PubMed1993

Assessment of autonomic function in patients with neurally mediated syncope: augmented cardiopulmonary baroreceptor responses to graded orthostatic stress.

OBJECTIVES: The purpose of this study was to assess vagal tone and cardiopulmonary baroreceptor activity in patients with tilt-induced neurally mediated syncope. BACKGROUND: The causes of individual susceptibility to orthostatic stress leading to recurrent neurally mediated syncope remain obscure. The trigger for sympathetic withdrawal and increased vagal activity is believed to be stimulation of ventricular mechanoreceptors. METHODS: Seventeen patients (mean age 50.6 years) with recurrent syncope and a positive response on a 45-min 60 degrees head-up tilt test were compared with a control group of 17 patients (mean age 47.5 years) with unexplained syncope and negative tilt test findings. Vagal activity was assessed by high pressure baroreceptor testing and by temporal and spectral analysis of heart rate variability during Holter ambulatory electrocardiographic monitoring. Cardiopulmonary baroreceptor sensitivity was assessed by measurement of forearm vascular responses to lower body negative pressure. RESULTS: Mean high pressure baroreceptor sensitivity was 16.4 +/- 12.2 ms/mm Hg in the group with a positive tilt test response compared with 15.1 +/- 13.0 ms/mm Hg in the control group (p = NS). There were no significant differences between the groups in any of the temporal or spectral measures of heart rate variability. The increase in forearm vascular resistance in response to lower body negative pressure was 11.5 +/- 14.2 U in patients with tilt-induced syncope and 3.5 +/- 3.2 U in the control group at -5 mm Hg, 16.8 +/- 18.6 U and 4.8 +/- 5.3 U, respectively, at -10 mm Hg and 26.4 +/- 24.3 U and 10.2 +/- 7.8 U, respectively, at -20 mm Hg (p < 0.001). CONCLUSIONS: Patients with tilt-induced neurally mediated syncope have augmented cardiopulmonary baroreceptor responses to orthostatic stress. This finding sheds new light on the etiology of neurally mediated syncope.

Adult↗
PubMed1993

Atrial adaptive rate pacing in sick sinus syndrome: effects on exercise capacity and arrhythmias.

OBJECTIVE: To test the hypotheses that adaptive rate atrial (AAIR) pacing: significantly increases maximal exercise capacity, and results in significant suppression of supraventricular and ventricular arrhythmia compared with fixed rate atrial (AAI) pacing. DESIGN: Prospective, randomised, single blind, crossover study with maximal treadmill exercise testing and 24 hour ambulatory electrocardiographic monitoring in AAIR and AAI modes. SETTING: Regional pacing centre. PATIENTS: 30 consecutive patients (mean SD age 65 (12) years) with sick sinus syndrome who required permanent pacing, without evidence of conduction disturbance on 12 lead electrocardiograms or 24 hour ambulatory electrocardiographic monitoring and without other cardiovascular or systemic disease. INTERVENTIONS: Activity sensing or minute ventilation driven systems (AAI/AAIR) were implanted alternately. RESULTS: The mean (SD) peak heart rate in AAI mode was 122(28)v 130(22) in AAIR mode (p < 0.02) for the whole group and 104(17) v 120(5) (p < 0.003) for the patients with chronotropic incompetence. Exercise time was 12.3 (4.1) minutes in AAI and 12.3 (3.8) minutes in AAIR mode (NS) in the chronotropically incompetent patients. There were no significant differences in the Borg scores at peak exercise in AAI v AAIR mode in either group. The frequency per hour of atrial and ventricular arrhythmias showed no significant differences between the two modes in either the group as a whole or in the subgroups with chronotropic incompetence. CONCLUSION: AAIR pacing confers little benefit in sick sinus syndrome compared with AAI pacing.

Aged↗
PubMed1993

Increased renal and forearm vasoconstriction in response to exercise after heart transplantation.

OBJECTIVE: To test the hypothesis that the loss of the inhibitory effect of the cardiac ventricular afferent fibres on the vasomotor centre would result in increased vasoconstrictor drive to the forearm and renal vascular beds during supine exercise in heart transplant recipients. DESIGN: Comparison of regional haemodynamic response to exercise in heart transplant recipients and two age matched control groups. SETTING: Regional heart transplant unit. PATIENTS AND METHODS: Orthotopic heart transplant recipients (n = 10), patients with NYHA class II heart failure (n = 10), and normal controls (n = 10) underwent short duration maximal supine bicycle exercise. MAIN OUTCOME MEASURES: Simultaneous measurements were made of heart rate, systemic blood pressure, oxygen consumption (VO2), forearm blood flow, and renal blood flow. Forearm blood flow was measured by forearm plethysmography and renal blood flow by continuous renal vein thermodilution. RESULTS: The peak forearm vascular resistance was significantly greater in the transplant group than in the controls (mean (SEM) 75 (18) v 40 (7) resistance units, p < 0.05). The percentage fall in renal blood flow at peak exercise was significantly greater in heart transplant recipients than in the controls (44% (4%) v 32% (4%), p < 0.05) as was the percentage increase in renal vascular resistance (transplants: 116% (19%) v controls: 78% (17%), p < 0.05). Regional haemodynamics during exercise in the heart failure group were not significantly different from those in the controls. CONCLUSIONS: These findings suggest that surgical division of the cardiac ventricular afferent fibres results in increased vasoconstrictor drive to the kidneys and non-exercising muscle during exercise. This mechanism may contribute to persistent exercise limitation and renal impairment after heart transplantation.

Adult↗
PubMed1993

Assessment of heart rate variability in hypertrophic cardiomyopathy. Association with clinical and prognostic features.

BACKGROUND: Altered vascular responses during exercise and disturbed responses to autonomic function testing have been documented in hypertrophic cardiomyopathy (HCM) and are associated with markers of an adverse prognosis. Reduced heart rate variability (HRV) and baroreflex sensitivity are predictors of increased risk of sudden death after myocardial infarction, but the value of these parameters in HCM is unknown. METHODS AND RESULTS: To determine the clinical significance of HRV and its relation to markers of electrical and hemodynamic instability in HCM, the 24-hour Holter recordings of 104 patients in sinus rhythm and off medication were analyzed. Five nonspectral measures of HRV were computed. The frequency components of HRV were calculated by fast Fourier transformation of the RR time intervals; the areas under the low (0.04 to 0.15 Hz) and high (0.15 to 0.4 Hz) frequency portions of the spectrum were measured as indices of autonomic and specific vagal influences on HRV, respectively. Spectral and nonspectral measures were compared with clinical, echo/Doppler, and Holter variables. ANCOVA was performed to allow for the effect of age on differences between variables. Spectral and nonspectral measures of HRV were correlated (r > .65; P < or = .001), indicating that the different time-domain and frequency parameters reflected similar measures of HRV. Global measures of HRV including the standard deviation of the mean of RR intervals (SDRR) and the standard deviation of 5-minute mean RR intervals (SDANN) were increased in patients with an adverse family history of HCM (173 +/- 67 vs 131 +/- 38 milliseconds, P = .001, and 158 +/- 66 vs 116 +/- 36 milliseconds, P = .004, respectively). In patients with exertional chest pain, global nonspectral measures were reduced compared with asymptomatic patients (118 +/- 31 vs 152 +/- 53 milliseconds, P = .006, and 105 +/- 30 vs 136 +/- 52 milliseconds, P = .014, respectively). Specific vagal influences on HRV including the proportion of RR intervals more than 50 milliseconds different (PNN50) and the high frequency peak on spectral analysis were less in patients with supraventricular arrhythmias on Holter monitoring (7.2 +/- 8 vs 16 +/- 13%, P = .012, and 21 +/- 10 vs 28 +/- 13 milliseconds, P = .048, respectively). Similarly, both global and specific vagal measures of HRV were less in the 27 patients with nonsustained ventricular tachycardia on Holter (PNN50, 7.7 +/- 9 vs 15 +/- 13 milliseconds, P = .048, and high frequency component, 19 +/- 9 vs 28 +/- 13 milliseconds, P = .05. During follow-up, 10 patients, 9 of whom were aged less than 33 years, experienced catastrophic events; 6 were resuscitated from ventricular fibrillation and 4 died suddenly. Indices of HRV were similar in these 10 patients to indices in the 94 survivors. CONCLUSIONS: Time-domain and spectral measures of HRV yield similar information about the specific autonomic influences on the heart. Global and specific vagal influences on HRV were reduced in patients with symptoms and arrhythmias and global HRV is increased in patients with an adverse family history of HCM, but these indices do not add to the predictive accuracy of established risk factors.

Adult↗