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At least 397 records · Page 22Linked to original sources
PubMed1998

Effect of flecainide on heart rate variability in subjects without coronary artery disease or congestive heart failure.

Heart rate variability is a noninvasive indicator of autonomic nervous system activity. The role of the autonomic nervous system in the genesis of atrial or ventricular arrhythmias is now well established. Little is known about the effects of flecainide on heart rate variability in patients with normal heart structure, the main population receiving flecainide. This study was designed to evaluate the effects of flecainide on heart rate variability in patients without coronary artery disease or congestive heart failure. Time and frequency domain analysis of heart rate variability on 24-hour electrocardiogram recording were assessed in 40 patients with normal echocardiography and without evidence of coronary artery disease before and after 2 months of oral treatment with flecainide (321 +/- 57 mg/day) prescribed for Wolff Parkinson White syndrome with circus movement tachycardia. Flecainide significantly decreased all parameters of heart rate variability in the time domain (median delta% -10% to -25%) and in the frequency domain (median delta% -27% to -38%), including the markers of vagal activity. There was no correlation between plasma concentrations of flecainide and reduction in heart rate variability. It was concluded that in subjects without coronary artery disease or congestive heart failure, flecainide decreases all the measurements of heart rate variability and this decrease is not related to plasma concentrations of flecainide.

Adolescent↗
PubMed2006

Engineered heart tissue grafts improve systolic and diastolic function in infarcted rat hearts.

The concept of regenerating diseased myocardium by implantation of tissue-engineered heart muscle is intriguing, but convincing evidence is lacking that heart tissues can be generated at a size and with contractile properties that would lend considerable support to failing hearts. Here we created large (thickness/diameter, 1-4 mm/15 mm), force-generating engineered heart tissue from neonatal rat heart cells. Engineered heart tissue formed thick cardiac muscle layers when implanted on myocardial infarcts in immune-suppressed rats. When evaluated 28 d later, engineered heart tissue showed undelayed electrical coupling to the native myocardium without evidence of arrhythmia induction. Moreover, engineered heart tissue prevented further dilation, induced systolic wall thickening of infarcted myocardial segments and improved fractional area shortening of infarcted hearts compared to controls (sham operation and noncontractile constructs). Thus, our study provides evidence that large contractile cardiac tissue grafts can be constructed in vitro, can survive after implantation and can support contractile function of infarcted hearts.

Animals↗
PubMed1996

Reproducibility of heart rate variability measures in patients with chronic heart failure.

1. In patients with chronic heart failure, heart rate variability is reduced with relative preservation of very-low-frequency power (< 0.04 Hz). Heart rate variability has been measured without acceptable information on its stability and the optimal recording periods for enhancing this reproducibility. 2. To this aim and to establish the optimal length of recording for the evaluation of the very-low-frequency power, we analysed 40, 20, 10 and 5 min ECG recordings obtained on two separate occasions in 16 patients with chronic heart failure. The repeatability coefficient and the variation coefficient were calculated for the heart rate variability parameters, in the time-domain (mean RR, SDRR and pNN50), and in the frequency-domain: very low frequency (< 0.04 Hz), low frequency (0.04-0.15 Hz), high frequency (0.15-0.40 Hz), total power (0-0.5 Hz). 3. Mean RR remained virtually identical over time (variation coefficient 8%). The reproducibility of time-domain (variation coefficient 25-139%) and of spectral measures (variation coefficient 45-111%) was very low. The stability of the heart rate variability parameters was only apparently improved after square root and after log transformation. 4. Very-low-frequency values derived from 5 and 10 min intervals were significantly lower than those calculated from 40 and 20 min intervals (P < 0.005). Discrete very-low-frequency peaks were detected in 11 out of 16 patients on the first 40, 20 and 10 min recording, but only in seven out of 16 when 5 min segments were analysed. 5. The reproducibility of both time or frequency-domain measures of heart rate variability in patients with chronic heart failure may vary significantly. Square root or log-transformed parameters may be considered rather than absolute units in studies assessing the influence of management on heart rate variability profile. Recordings of at least 20 min in stable, controlled conditions are to be recommended to optimize signal acquisition in patients with chronic heart failure, if very-low-frequency power in particular is to be studied.

Chronic Disease↗
PubMed2002

Cumulative effect of complete left bundle-branch block and chronic atrial fibrillation on 1-year mortality and hospitalization in patients with congestive heart failure. A report from the Italian network on congestive heart failure (in-CHF database).

BACKGROUND: Many clinical variables have been proposed as prognostic factors in patients with congestive heart failure. Among these, complete left bundle-branch block and atrial fibrillation are known to impair significantly left ventricular performance in patients with congestive heart failure. However, their combined effect on mortality has been poorly investigated. The aim of this study was to determine whether left bundle-branch block associated with atrial fibrillation had an independent, cumulative effect on mortality for congestive heart failure. METHODS AND RESULTS: We analysed the Italian Network on congestive heart failure (IN-CHF) Registry that was established by the Italian Association of Hospital Cardiologists in 1995. One-year follow-up data were available for 5517 patients. Complete left bundle-branch block and atrial fibrillation were associated in 185 (3.3%) patients. In this population the cause of congestive heart failure was dilated cardiomyopathy (38.4%), ischaemic heart disease (35.1%), hypertensive heart disease (17.3%), and other aetiologies (9.2%). This combination of electrical defects was associated with an increased 1-year mortality from any cause (hazard ratio, HR: 1.88; 95% CI 1.37-2.57) and sudden death (HR: 1.89; 95% CI 1.17-3.03) and 1-year hospitalization rate (HR: 1.83; 95% CI 1.26-2.67). CONCLUSIONS: In patients with congestive heart failure, the contemporary presence of left bundle-branch block and atrial fibrillation was associated with a significant increase in mortality. This synergistic effect remained significant after adjusting for clinical variables usually associated with advanced heart failure. We can conclude that this combination of electrical disturbances identifies a congestive heart failure specific population with a high risk of mortality.

Adolescent↗
PubMed2002

Heart rate recovery after exercise is related to the insulin resistance syndrome and heart rate variability in elderly men.

OBJECTIVE: We investigated the associations between heart rate recovery after exercise (as a suggested measure of vagal activity), heart rate variability, and measurements of the insulin resistance syndrome. MATERIAL AND METHODS: Seventy men aged 70 years were examined with a symptom-limited bicycle exercise test, a 24-hour heart rate variability test, and different measurements of different components of the insulin resistance syndrome. RESULTS: Heart rate recovery after exercise (mean +/- SD 20 +/- 9 beats during the first minute) was related to both the SD of the R-R interval and the low frequency power at the heart rate variability analyses (r = 0.39, P <.002 for both). Furthermore, heart rate recovery after exercise was related to insulin sensitivity at the hyperinsulinemic eugleucemic clamp (r = 0.28, P <.03), and to high-density lipoprotein cholesterol and exercise capacity, and inversely to obesity and insulin and glucose levels 2 hours after an oral glucose load (P <.05 for all). Heart rate recovery after exercise was not related to left ventricular mass measured by means of echocardiography or to the number of ventricular premature complexes at a 24-hour Holter recording. CONCLUSION: Heart rate recovery 1 minute after exercise was related to measurements of 24-hour heart rate variability. Furthermore, heart rate recovery after exercise was related to several of the major components of the insulin resistance syndrome, thereby establishing a link between this syndrome and cardiac autonomic nervous activity.

Age Factors↗
PubMed1996

Determinants of heart rate variability in heart transplanted subjects during physical exercise.

Respiratory sinus arrhythmia has been described in heart transplanted subjects. In order to investigate the mechanisms involved in the generation of this condition in the transplanted heart and its evolution after surgery, graded exercise was performed (0-75 W in 25 W steps) on a cycle ergometer by 41 subjects (mean age 44 years) who had undergone heart transplantation 28 months (range 3-60) earlier and by six age matched-control subjects. R-R interval, respiratory signal, O2 consumption (VO2) and CO2 production (VCO2) were measured. Respiratory sinus arrhythmia was assessed by the autoregressive power spectrum of the R-R interval and respiration. All subjects reached the anaerobic threshold (heart transplants: 60% at 50 W, 40% at 75 W Controls: 150 W). In control subjects, the respiratory sinus arrhythmia was higher than in heart transplanted subjects (5.80 +/- 0.30 vs 1.45 +/- 0.16 1n ms2) and it decreased significantly (4.66 +/- 0.30 1n ms2, P < 0.05) during exercise, despite the increase in breathing rate and depth. When, the group of heart transplanted subjects was considered as a whole, respiratory sinus arrhythmia was found to be present in all conditions. It significantly increased at 25 W (from 1.45 +/- 0.16 to 2.00 +/- 0.17 1n ms2, P < 0.01), then significantly fell below baseline during recovery (to 0.97 +/- 0.23 1n ms2, P < 0.01). Multiple regression analysis showed that a linear combination of heart rate (inverse correlation) and VO2 (direct correlation) together with months having passed since transplantation surgery, could explain the observed changes in heart rate during exercise (multiple regression: r = 0.658, P < 0.0001). In five long-term transplanted subjects, non respiratory-related low frequency (0.1 Hz) waves were present on the R-R spectrum, but respiratory sinus arrhythmia is also present in the recently transplanted heart and depends on the opposing effects of ventilation and heart rate. In a few cases, sympathetic modulation (re-innervation) could not be excluded.

Adult↗
PubMed1996

Circadian variations of blood pressure and heart rate early and late after heart transplantation.

Cardiac reinnervation late after heart transplantation has been reported in individual patients. As a measure for reinnervation, circadian changes in arterial blood pressure and heart rate have been used but not yet systemically evaluated in cardiac transplant recipients. Ambulatory blood pressure and heart rate monitoring was performed in 62 patients for 24 hr early (<6 months, mean 26 days, range 5-90 days, n=30) and late (> or = 6 months, mean 12 months, range 7-78 months, n=32) after heart transplantation. A loss of physiological nocturnal decline in blood pressure and heart rate was noted early after transplantation, whereas late after operation an improvement in circadian changes of blood pressure and heart rate was observed. The patients late after heart transplantation had a significant higher diastolic blood pressure. A pathological circadian blood pressure and heart rate pattern was observed in patients early after heart transplantation, which was improved late after operation. This could be explained by partial reinnervation of the heart. Diastolic hypertension late after transplantation may be due to cyclosporine treatment and/or neuroendocrine hyperactivity.

Adult↗
PubMedDate not supplied

Congestive heart failure and continuous positive airway pressure therapy: support of a new modality for improving the prognosis and survival of patients with advanced congestive heart failure.

Nasal continuous positive airway pressure therapy has recently been studied as a nonpharmacologic adjunct to congestive heart failure therapy. In patients with congestive heart failure, it was reported that continuous positive airway pressure therapy for the condition Cheyne-Stokes respiration with central sleep apnea led to long-term improvements in cardiac function and alleviation of heart failure symptoms. Cheyne-Stokes respiration with central sleep apnea is a frequent breathing disorder well described in patients with congestive heart failure, and is an associated risk factor for increased cardiovascular morbidity and mortality. These apneas cause an increase in sympathetic nervous system activity, which would maintain afterload at a high level or tend to increase it with time, leading to further compromise of ejection fraction. Continuous positive airway pressure appears to benefit the failing heart by increasing intrathoracic pressure, which is believed to cause an increase in cardiac output by decreasing the pressure gradient across the heart wall and allowing the left-ventricular end diastolic volume to decrease, thereby reducing the afterload. This beneficial "resting" of the heart has been documented to increase left-ventricular ejection fraction, increase cardiac index, improve inspiratory muscle strength, lower blood pressure and heart rate, decrease plasma and overnight urinary levels of norepinephrine, lower levels of atrial natriuretic peptide and endothelin-1, and increase heart rate variability. Other benefits include improvement in New York Heart Association functional class status and improvement in dyspnea.

Adult↗
PubMed2006

Pacemaker implantation as a risk factor for heart failure in young adults with congenital heart disease.

AIM: Complete postoperative heart block following open-heart surgery and sinus node dysfunction are indications for permanent cardiac pacing in children with congenital heart defects. The purpose of our study was to evaluate if cardiac pacing is a risk factor of heart failure during longtime follow-up of grown ups with congenital heart disease (GUCH). METHODS: For an objective assessment of heart failure, NT-Pro brain natriuretic peptide (BNP) and maximal oxygen uptake index (VO2max) during the cardiopulmonary exercise testing were measured in 346 consecutive GUCH patients during a longtime follow-up examination. RESULTS: Thirty-nine of these patients who had pacemaker implantation had significantly increased BNP levels (448.2 +/- 76.8 vs 123.8 +/- 9.7 pg/mL, P < 0.0001) and significantly decreased VO(2max) (22.5 +/- 0.9 vs 27.4 +/- 0.4, P < 0.0001). Heart failure in pacemaker patients was associated with significantly prolonged QRS complex durations (171.1 +/- 8.3 ms vs 108.7 +/- 1.8 ms, P < 0.0001), increased right ventricular end diastolic diameters (38.7 +/- 2.1 mm vs 27.8 +/- 0.5mm, P < 0.0001), lower heart rates at rest (69.5 +/- 1.9/min vs 82 +/- 1/min, P < 0.0001), and at exercise (140.3 +/- 5.8/min vs 163.5 +/- 1.2/min, P < 0.0001). Mean fractional shortening of the left ventricle was normal in both patient groups. CONCLUSION: Pacemaker implantation may be associated with heart failure during longtime follow-up of GUCH indicated by significantly elevated BNP levels and decreased VO2max. Possible explanations are prolongation of QRS complex duration, decreased maximal heart rates during exercise, and dilatation of the right ventricle.

Adult↗
PubMed1987

The mitochondrial adenosine 5'-triphosphatase in slow and fast heart rate hearts.

A survey of 12 species has revealed that reversible ischemia-induced protonic inhibition of the cardiac muscle mitochondrial adenosine 5'-triphosphatase (ATPase) described by this author earlier (Rouslin, W. J. Biol. Chem. 258: 9657-9661, 1983) occurs only in animals with heart rates lower than approximately 200 beats/min. It was thus fully demonstrable in rabbit, dog, sheep, human, pig, and beef heart mitochondria. In contrast, the in situ ATPase inhibition was completely absent in six smaller species capable of heart rates of approximately 300 or more beats/min. These were chicken, pigeon, guinea pig, rat, hamster, and mouse. Analyses of the cardiac muscle mitochondria of 9 of the 12 species studied showed them to contain normal levels of mitochondrial ATPase inhibitor; the three smallest species, rat, hamster, and mouse contained only very low levels of inhibitor. Thus, although chicken, pigeon, and guinea pig heart mitochondria contained normal levels of ATPase inhibitor, they (like the rat, hamster, and mouse) showed no in situ ischemia-induced ATPase inhibition. This and other observations suggest that the lack of in situ ATPase inhibition in hearts capable of 300 or more beats/min may be due to the presence of either an in situ nonfunctional ATPase inhibitor protein or to an in situ uninhibitable form of the mitochondrial ATPase in the faster-paced hearts. Alternatively, the mitochondria of the fast-paced hearts may be insulated somehow against the cytosolic acidosis which develops during ischemia and which triggers the ATPase inhibition in the slow heart-rate hearts. In the faster paced hearts, ATP hydrolysis does not appear to be regulated by inhibitor binding to the ATPase under nonenergizing conditions.

Adenosine Triphosphatases↗
PubMed1993

Nonlinear heart model predicts range of heart rates for 2:1 swinging in pericardial effusion.

We analyze two mathematical models of Rigney and Goldberger (14) of heart swinging in large pericardial effusions. Both models represent the torques due to the outflow of blood from the heart. The first assumes that the duration of systole does not vary with heart rate (in beats/min), whereas the second assumes that it varies linearly with heart rate. We examine the motion of the heart for heart rates between 50 and 200 and for a range of initial positions and velocities. Both models predict that the heart swings once every other beat (2:1 swinging, giving rise to electrical alternans) in a discrete range of heart rates and swings once per beat otherwise; both models explain the appearance and disappearance of 2:1 swinging mathematically. The first model predicts a rate range from 105 to 116 for the occurrence of 2:1 swinging. The second model predicts the same qualitative behavior but with 2:1 swinging occurring at heart rates between 88 and 119, which agrees well with published clinical data showing 2:1 swinging at heart rates between 90 and 144. We describe an analysis program for ordinary differential equations that analyzed the models quickly and automatically.

Animals↗
PubMed2002

The heart of Ciona intestinalis: eicosanoid-generating capacity and the effects of precursor fatty acids and eicosanoids on heart rate.

Eicosanoids are a group of oxygenated fatty-acid derivatives formed from C20 polyunsaturated fatty acids including arachidonic and eicosapentaenoic acids. In mammals, these compounds have been shown to be key molecules in several physiological processes including regulation of the vascular system. This study determined whether eicosanoids or their precursors are involved in the regulation of heart rate in the sea squirt Ciona intestinalis. Eicosanoid generation by both heart and blood cells was measured. The major lipoxygenase products formed were both derivatives of eicosapentaenoic acid, namely 8- and 12-hydroxyeicosapentaenoic acids (8-HEPE and 12-HEPE). Smaller amounts of 8,15-dihydroxyeicosapentaenoic acid (8,15-diHEPE) were also formed. The cyclo-oxygenase product prostaglandin E was also found in small amounts in the heart. Isolated hearts were exposed either to these fatty acid precursors or to 8-HEPE, 12-HEPE or prostaglandin E3, and the effect on heart rate was recorded. Both eicosapentaenoic and arachidonic acids stimulated the heart rate at concentrations between 50 and 200 micromol l(-1). 12-HEPE (5 micromol l(-1)) and prostaglandin E3 (50 micromoll(-1)) caused a modest increase in heart rate, while 8-HEPE had no significant effects at any of the time periods studied (<or=180 min). Overall, the results show that arachidonic and eicosapentaenoic acids have limited effects on heart rate and only at concentrations unlikely to be routinely liberated in vivo. Similarly, the eicosanoids tested had a minor stimulatory activity on heart rate. The potential mechanisms for this stimulation are discussed. Overall, these results suggest that such compounds are of limited importance in regulating the heart and vascular system of sea squirts.

Animals↗
PubMed1992

Changes in endocrine control of electrolyte homeostasis and blood pressure following heart and heart-lung transplantation. A comparative study.

The purpose of this study was to compare the early postoperative effects of heart and heart-lung transplantation on the secretion of atrial natriuretic peptide (alpha-ANP), renin, aldosterone, and vasopressin. This was carried out from the first to the eighth postoperative day in ten heart and five heart-lung recipients. The changes in the release of these hormones were similar in both groups. Vasopressin release remained stable while that of the renin-angiotensin-aldosterone system progressively returned to more normal levels. Grafted heart tissue was capable of high alpha-ANP release early on in both heart and in heart-lung recipients. This sustained alpha-ANP release was not a function of the resulting overall atrial tissue mass. Our findings suggest that it might be the consequence of an intrinsic hypersecretion of alpha-ANP resulting from the loss of normal heart innervation occurring in both heart and heart-lung transplantation.

Adult↗
PubMed2004

Heart and liver disease in 32 patients undergoing biopsy of both organs, with implications for heart or liver transplantation.

OBJECTIVE: To determine underlying conditions in patients undergoing both heart and liver biopsies. PATIENTS AND METHODS: Our study group consisted of 32 patients at the Mayo Clinic in Rochester, Minn, who underwent both endomyocardial and nonsurgical liver biopsies and who underwent at least one of these procedures between January 1,1981, and December 31,2000. Patients were categorized as having (1) heart disease affecting the liver, (2) liver disease affecting the heart, (3) the same disease affecting both organs, or (4) different diseases affecting each organ independently. RESULTS: Among 32 patients, cardiac dysfunction was present in 28 (19 systolic, 9 diastolic), and hepatic dysfunction was present in 31. In group 1, 3 of 4 patients had cardiac amyloidosis with secondary hepatic congestion. In group 2, all 3 patients had cirrhosis with cirrhotic cardiomyopathy. Group 3 included 5 patients with hemochromatosis, 3 with alcoholism, and 1 with amyloidosis. In group 4, 8 of 16 patients had idiopathic cardiomyopathy, and 8 had hepatitis. Overall, of 8 patients with hemochromatosis, 3 without cardiac iron had improved cardiac function after phlebotomy, and 1 with cardiac iron had no cardiac dysfunction. Among 7 patients with alcoholism, 3 had alcoholic liver and heart disease. Of 5 patients with cardiac amyloidosis, 1 had hepatic amyloid. Ten patients underwent transplantation (6 liver, 3 heart, and 1 heart and liver). CONCLUSIONS: In one half of the patients in the study group, heart and liver diseases had independent causes. In patients with hemochromatosis, there was little correlation between cardiac iron and systolic dysfunction. In patients with chronic alcoholism, liver and heart disorders often had nonalcoholic causes. With cardiac amyloidosis, hepatic dysfunction was generally due to congestion. Specific disease in one organ did not necessarily imply similar involvement in the other. Thus, heart or liver biopsy may be useful in patients being evaluated for liver or heart transplantation, respectively.

Adolescent↗
PubMed1992

Baroreflex control of heart rate in rats with heart failure after myocardial infarction: effects of captopril.

Activation of the renin-angiotensin and sympathetic nervous systems in heart failure may result in altered baroreflex control of heart rate. To determine the specific effects of treatment with captopril on baroreceptor dysfunction in heart failure, baroreflex control of heart rate was measured in conscious rats with heart failure 6 weeks after ligation of the left coronary artery. Plasma norepinephrine was measured as a reflection of sympathetic nervous system activity. After bolus injections of phenylephrine (2-50 micrograms/kg) and nitroprusside (2-50 micrograms/kg), the arterial baroreflex was analyzed by fitting percentage of mean arterial pressure changes and heart rate changes to a logistic regression function. There were no differences in baroreflex function between normal and sham-operated rats. Plasma norepinephrine was increased (P < .05) in the heart-failure rats and did not change with captopril treatment. In untreated rats, heart failure increased (P < .05) the centering point by 900%, threshold by 243% and saturation by 89%, whereas decreasing (P < .05) the operational point by 73%. There was a decrease (P < .05) in the nitroprusside-related gain and an increase (P < .05) in phenylephrine-related gain, but the overall baroreflex gain was not changed. In heart-failure rats, captopril increased (P < .05) threshold, saturation and centering point and decreased (P < .05) operational point and nitroprusside- and phenylephrine-related gain abnormalities. The increase in operational point and decreases in threshold, saturation, centering point and phenylephrine-related gain were the results of a specific interactive effect of captopril in heart failure (P = .0033, .0176, .0509, .0217 and .0567, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Isoproterenol-produced damage in amphibian heart could be mediated by adrenergic receptors located in the heart muscle.

In mammals, isoproterenol may produce heart damage in part by binding to adrenergic receptors in the coronary arteries. Previously we showed evidence that isoproterenol produces cellular necrosis and interstitial fibrosis in the ventricle of the heart of an amphibian, which has no coronary arteries. The present study examines responses to 3-adrenergic receptor stimulation in the heart of urodele amphibians. The hearts from three amphibians; Ambystoma mexicanum, A. tigrinum and A. dumerilii were mounted in an organ bath at 16+/-2 degrees C. The spontaneous isometric contractions (heart rate and isometric tension) were recorded using a tension transducer connected to polygraph. Concentration-response to isoproterenol in the presence and absence of propranolol (10(-6)) was recorded. The basal heart rate in the A. mexicanum heart was 19+/-2 beats/min and in A. tigrinum and A. dumerilii was 14+/-2 beats/min. The auricular tension was 284+/-15, 190+/-10, 140+/-8 mg, while the ventricular tension was of 62+/-3, 55+/-2 and 29+/-2 mg for A. mexicanum, A. tigrinum and A. dumenrilii respectively. Isoproterenol (10(-9), 10(-6), 10(-3) M) increased the heart rate and tension in a dose-dependent manner, and the effect was reversed in presence of propranolol. Our results indicate that isoproterenol-induced heart damage in urodele amphibians can be mediated by beta-adrenergic receptors located in the heart muscle. In the future, it will be necessary to characterize adrenergic receptor subtypes directly in these species, in order to understand the mechanism underlying the use of isoproterenol in experimental models of cardiac injury in non- mammalian vertebrates.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Cytoimmunologic monitoring after heart and heart-lung transplantation.

The ability of cytoimmunologic monitoring to detect acute rejection in heart and heart-lung transplant recipients was assessed. Seventeen heart and nine heart-lung transplant patients treated with cyclosporine as the primary immunosuppressive agent were monitored after operation. Seventeen acute rejection episodes occurred in the heart-only recipients and 12 in the combined heart-lung recipients. These acute rejection reactions were accompanied by increased numbers of "activated" lymphocytes in all but one case, providing cytoimmunologic monitoring a sensitivity of 100% in the heart-lung recipients and 94% in the heart recipients. The specificity was, however, low (68% in the heart recipients and 55% in the heart-lung recipients). Seventy-two percent of the false-positive results were associated with viral infections, particularly cytomegalovirus infections.

Adolescent↗
PubMedDate not supplied

DHPG effectively treats CMV infection in heart and heart-lung transplant patients: a preliminary report.

Cytomegalovirus (CMV) infection in heart and heart-lung transplant recipients represents a serious if not mortal complication. This study reviews the beneficial effects of 9-(1,3-dihydroxy-2-proproxymethyl) guanine (DHPG), an experimental antiviral agent, in patients with CMV infections. Thirteen of 76 heart and heart-lung transplant patients treated with cyclosporine have developed CMV. Nine of 13 patients developed infections since DHPG has been available. Seven patients received hearts, and two received heart and lungs. Six patients were treated, four heart and two heart-lung recipients; five of six had negative CMV serology before surgery, and all had CMV positive donors. Of the patients not treated, one died at home from disseminated CMV; two had resolution of symptoms and were discharged before the diagnosis was made. In the treated group, three patients had gastrointestinal ulcerative disease, two in the stomach and one in the cecum. The other three patients had CMV pneumonia. DHPG was effective in resolving patient symptoms in five of six patients. The patient who did not respond had a cecal ulcer, multiorgan failure, multiple infections, and died. Two patients with abdominal pain had gastric ulcers that were proved with endoscopy. CMV-induced ulcer disease was diagnosed within 2 hours by fluorescent antibody staining, and resolution was documented by endoscopy. Three patients with CMV pneumonia were treated; two were heart-lung transplant recipients. All started to respond within 72 hours. One heart-lung transplant recipient has had a 9-month course of DHPG because of recurrence of infection when the drug was stopped. The usual dosage was 10 mg/kg/day over 2 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)

Acyclovir↗