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Biomedical subjects

M Haass

Publications and source records attributed to M Haass.

At least 37 records · Page 2Linked to original sources
PubMed2001

Risk stratification in middle-aged patients with congestive heart failure: prospective comparison of the Heart Failure Survival Score (HFSS) and a simplified two-variable model.

AIMS: The performance of a US-American scoring system (Heart Failure Survival Score, HFSS) was prospectively evaluated in a sample of ambulatory patients with congestive heart failure (CHF). Additionally, it was investigated whether the HFSS might be simplified by assessment of the distance ambulated during a 6-min walk test (6'WT) instead of determination of peak oxygen uptake (peak VO(2)). METHODS AND RESULTS: In 208 middle-aged CHF patients (age 54+/-10 years, 82% male, NYHA class 2.3+/-0.7; follow-up 28+/-14 months) the seven variables of the HFSS: CHF aetiology; heart rate; mean arterial pressure; serum sodium concentration; intraventricular conduction time; left ventricular ejection fraction (LVEF); and peak VO(2), were determined. Additionally, a 6'WT was performed. The HFSS allowed discrimination between patients at low, medium and high risk, with mortality rates of 16, 39 and 50%, respectively. However, the prognostic power of the HFSS was not superior to a two-variable model consisting only of LVEF and peak VO(2). The areas under the receiver operating curves (AUC) for prediction of 1-year survival were even higher for the two-variable model (0.84 vs. 0.74, P<0.05). Replacing peak VO(2) with 6'WT resulted in a similar AUC (0.83). CONCLUSION: The HFSS continued to predict survival when applied to this patient sample. However, the HFSS was inferior to a two-variable model containing only LVEF and either peak VO(2) or 6'WT. As the 6'WT requires no sophisticated equipment, a simplified two-variable model containing only LVEF and 6'WT may be more widely applicable, and is therefore recommended.

Adult↗
PubMed2001

Echocardiographic quantification of left ventricular asynergy in coronary artery disease with Fourier phase imaging.

BACKGROUND: Visual evaluation of wall motion is subjective and may be difficult in patients with impaired left ventricular function. Current algorithms used to analyze wall motion usually neglect motion asynchrony that may be profoundly altered in coronary artery disease. This study was to investigate whether the extent of left ventricular asynergy can be used to quantify the severity of regional myocardial dysfunction by the use of Fourier phase imaging. METHODS: Echocardiographic cine loops of 21 patients with ischemic cardiomyopathy (EF < or = 40%) were mathematically transformed using a first-harmonic Fourier algorithm displaying the sequence of wall motion as phase angles in parametric images and regional phase histograms. Segmental fractional area shortening (FAC) and qualitative assessment of regional wall motion based on visual inspection served as reference method. RESULTS: There was an inverse linear relationship between FAC and phase angles (r = -0.75, p < 0.01). Normal endocardial motion yielded low phase angles (mean 16 +/- 15 degrees SD). With an increase in wall motion abnormalities, phase angles were progressively delayed by 56 +/- 38 degrees in hypokinetic, by 88 +/- 38 degrees in akinetic, and by 143 +/- 33 degrees (p < 0.001) in dyskinetic segments. CONCLUSIONS: These results demonstrate that left ventricular asynchrony is an indicator of regional myocardial dysfunction in coronary artery disease. Echocardiographic Fourier phase imaging can be used to quantify wall motion displaying contraction sequence in a simple and objective format.

Aged↗
PubMed2000

[The 6 minute walking test: a cost-effective alternative to spiro-ergometry in patients with chronic heart failure?].

In contrast to the often debated NYHA classification, the determination of peak oxygen uptake (peak VO2) by cardiopulmonary exercise testing allows an objective assessment of the exercise capacity of patients with congestive heart failure (CHF). However, cardiopulmonary exercise testing is a time consuming and costly diagnostic tool, which requires sophisticated equipment and specially trained personel. Exercise capacity can also be determined by the 6 minute walk test. This test simply measures the distance covered by strong walking on a hallway level within 6 minutes. The 6 minute walk test is a submaximal exercise test, which is associated with much smaller increments in heart rate, blood pressure and plasma catecholamines than cardiopulmonary exercise testing. It is characterized by a very small intraindividual variance. Furthermore, it can be easily performed and, due to low logistic and personal requirements, it is very cost effective. The results of the 6 minute walk test--as well as of cardiopulmonary exercise testing--are influenced by extracardial exercise-limiting disorders, such as pulmonary diseases. Independent from the etiology of CHF, the results of the 6 minute walk test are closely related to peak VO2. In serial exercise testing the distance covered within 6 minutes allow to predict the individual peak VO2. Like peak VO2 the 6 minute walk test has been shown to be a predictor of morbidity and mortality in CHF, with its predictive value being independent from left ventricular ejection fraction and other potential prognostic parameters. In CHF patients a walking distance < 300 m is associated with a one-year-mortality of up to 50%, whereas the one-year-mortality in patients reaching a walking distance > 450 m amounts to only a few percent. In addition, the hospitalization rate of patients reaching a walking distance of < 300 m is several fold higher than in those with a walking distance > or = 450 m. Like cardiopulmonary exercise testing, the 6 minute walk test allows to control the efficiency of specific treatments and to monitor the natural course of the disease. The 6 minute walk test is, thus, a cost effective alternative to cardiopulmonary exercise testing in CHF patients. However, neither the 6 minute walk test alone nor the results of cardiopulmonary exercise testing alone are sufficient for selecting patients, e.g., for cardiac transplantation, as each individual case requires a synopsis of all relevant facts and parameters.

Cardiomyopathy, Dilated↗
PubMed2000

Inefficient ventilation and reduced respiratory muscle capacity in congestive heart failure.

The extent and time-course of changes in lung volumes, ventilatory efficiency at rest and during exercise, and respiratory muscle function and their influence on exercise limitation in congestive heart failure (CHF) are unclear. It is unknown whether respiratory muscle function may predict changes in exercise limitation or may be impaired in patients with poor outcome. 145 male patients (54 +/- 1 years) suffering from CHF (NYHA class I-III, mean 2.3 +/- 0.1), with a LVEF of 23 +/- 1%, and a mean peak O2 uptake (VO2peak) 15.0 +/- 0.5 mL X min(-1) X kg(-1), were studied. They were grouped in Weber functional classes A to D according to their VO2peak. Significant increases in ventilatory equivalents for O2 and CO2 (VE/VCO2peak) and in dead space ventilation at rest and during exercise were found with increasing exercise limitation. Moreover, there was a correlation of static and dynamic lung volumes (inspiratory vital capacity, IVC, r = 0.43, P < 0.01), as well as of maximal inspiratory pressure (MIP; r = 0.46, P < 0.01) with VO2peak. Patients who died (n = 26) or were heart transplanted (n = 20) during a follow-up (mean 800 +/- 10 days) had a reduced MIP (6.4 +/- 0.4 kPa) as compared with survivors (n = 82; 9.3 +/- 0.7 kPa, P < 0.01). In a subgroup of 33 patients re-evaluated after six months, individual changes in IVC and VE/CO2peak, but not in MIP, correlated to changes in VO2peak (r = 0.69 and r = 0.72 respectively; P < 0.01). In CHF, exercise limitation is associated with reversible lung restriction and inefficient ventilation at rest and during exercise. Patients with severe CHF have a significant reduction in MIP, a finding that is associated with poor outcome.

Adult↗
PubMed2000

The bradycardic agent zatebradine enhances baroreflex sensitivity and heart rate variability in rats early after myocardial infarction.

OBJECTIVE: The bradycardic agent zatebradine (UL-FS 49) reduces heart rate without negative inotropic or proarrhythmic effects. The aim was to experimentally characterize the influence of zatebradine on arterial baroreflex sensitivity (BRS) and heart rate variability (HRV) which are generally considered as estimates of vagal activity and have prognostic value in patients after myocardial infarction (MI). METHODS: Conscious rats were studied 3 days after left coronary artery ligation or sham-operation (SH). BRS was determined by linear regression analysis of RR-interval and mean arterial pressure changes evoked by intravenous (i.v.) injections of methoxamine and nitroprusside. HRV at rest was calculated from high-resolution electrocardiogram-recordings. RESULTS: In MI-rats heart rate was similar to SH-rats, mean arterial pressure was lower and both BRS and HRV were markedly reduced. Zatebradine (0.5 mg/kg i.v.) reduced heart rate in MI-rats from 400 +/- 15 to 350 +/- 19 and in SH-rats from 390 +/- 19 to 324 +/- 6 beats/min without changing mean arterial pressure. Both BRS and HRV were restored in MI- and further increased in SH-rats by the drug. Effects of 0.05, 0.5 and 5 mg/kg zatebradine revealed a dose-dependency of heart rate reduction. The lowest dose enhanced reflex bradycardia despite little effect on heart rate and lack of effect on both reflex tachycardia and HRV. CONCLUSIONS: Both BRS and HRV are reduced in rats early after MI, indicating a depressed reflex and tonic vagal activity. Treatment with zatebradine enhances both BRS and HRV. These data suggest that the drug has both peripheral and central effects, leading to an increase of vagal control of heart rate.

Analysis of Variance↗
PubMed2000

Is the 6-minute walk test a reliable substitute for peak oxygen uptake in patients with dilated cardiomyopathy?

AIMS: The 6-min walk test may serve as a more simple clinical tool to assess functional capacity in congestive heart failure than determination of peak oxygen uptake by cardiopulmonary exercise testing. The purpose of the study was to prospectively examine whether the distance ambulated during a 6-min walk test (i) correlates with peak oxygen uptake, (ii) allows peak oxygen uptake to be predicted, and (iii) provides prognostic information similar to peak oxygen uptake in patients with dilated cardiomyopathy and left ventricular ejection fraction < or = 35%. METHODS AND RESULTS: In 113 patients (age: 54+/-12 years, NYHA: 2.2+/-0.8) with dilated cardiomyopathy (left ventricular ejection fraction 19+/-7%) a 6-min walk test and cardiopulmonary exercise testing were performed. The 6-min walk test and peak oxygen uptake were closely correlated at the initial visit (r=0.68, n=113), as well as after 263+/-114 (r=0.71, n=28) and 381+/-170 days (r=0.74, n=14). During serial exercise testing the 6-min walk test allowed peak oxygen uptake to be reliably predicted (r=0.76 between calculated and real peak oxygen uptake). After 528+/-234 days, 42 patients were hospitalized due to worsening heart failure and/or died from cardiovascular causes. Compared to clinically stable patients, these 42 patients walked a shorter distance (423+/-104 vs 501+/-95 m, P<0.001) and had a lower peak oxygen uptake (12.7+/-4.0 vs 17.4 + 5.6 ml x min(-1) x kg(-1), P<0.001). By univariate analysis the 6-min walk test outperformed other prognostic parameters such as left ventricular ejection fraction, cardiac index and plasma norepinephrine concentration and conferred a prognostic power similar to peak oxygen uptake. This predictive value could be further improved in a multivariate model, by combining the 6-min walk test with independent variables, such as left ventricular ejection fraction or cardiac index. CONCLUSION: The 6-min walk test correlated with peak oxygen uptake when tested serially over the course of the disease. Although both tests define two distinct domains of functional capacity, the 6-min walk test provides prognostic information very similar to peak oxygen uptake in congestive heart failure patients with dilated cardiomyopathy.

Aged↗
PubMed2000

HEp2 ANA EIA: a new fully automated assay for the screening of antinuclear antibodies.

BACKGROUND: Screening for antinuclear antibodies is performed for various systemic autoimmune diseases with various different techniques. A more recent approach to ANA screening is the use of enzyme immunoassays. OBJECTIVES: To introduce the new COBAS CORE HEp2 ANA EIA, the first fully automated enzyme immunoassay for the detection of ANA in serum and plasma of patients with suspected systemic autoimmune disease. METHODS: A method comparison between the new HEp2 ANA EIA and immunofluorescence assays on HEp2 cells was performed in two groups--977 patients with systemic autoimmune disorders and 952 healthy subjects with no autoimmune disease-related diagnosis. RESULTS: The clinical sensitivity in the patient group was 79.8% for HEp2 ANA EIA and 89.5% for IFA, and the clinical specificity in the control group was 91.7% for HEp2 ANA EIA and 93.9% for IFA. The analysis of 830 routine samples showed an overall good concordance of 85% between both assays. Further examination of the discrepant results showed 8% discrepant negative results for the HEp2 ANA EIA assay compared to 21% for IFA. Discrepant positive results were found in 37.9% and 33% of samples for the HEp2 ANA EIA and the IFA, respectively. CONCLUSION: The HEp2 ANA EIA is the first fully automated assay for the detection of ANA in serum and plasma. The assay shows improved sensitivity in ANA determination and a similar performance, compared to the standard method of IFA.

Antibodies, Antinuclear↗
PubMed1999

[Differential diagnosis in anorexia nervosa: glycogenosis II (the Pompe type)].

HISTORY AND ADMISSION FINDINGS: A 29-year-old woman had since early childhood been smaller and thinner than her contemporaries. Her weight was now 36.5 kg, height 158 cm. Anorexia nervosa being suspected she was to be admitted to a psychosomatic clinic. A few days before the date she developed respiratory failure which required mechanical ventilation for a month. Physical examination revealed markedly reduced musculature. INVESTIGATIONS: Muscle biopsy and fibroblast culture indicated acid maltase deficiency (glycogen storage disease Type II [Pompe's disease]). Lung functions were markedly reduced, blood gas analysis revealing global respiratory insufficiency. TREATMENT AND COURSE: Intermittent patient-controlled ventilation (at night by intermittent positive pressure ventilation) clearly improved both her general condition and blood gases. CONCLUSIONS: Acid maltase deficiency should be included as a possible cause of the differential diagnosis of anorexia nervosa. This diagnosis should strictly follow the criteria listed in ICD-10 (International Classification of Diseases), but also after exclusion of other causes.

Adult↗
PubMed1999

Influence of Bretschneider's cardioplegia on norepinephrine release from isolated perfused guinea-pig hearts.

It was the aim of the present study to investigate the influence of Bretschneider's cardioplegia on norepinephrine (NE) release [determined by high pressure liquid chromatography (HPLC) and electrochemical detection] in isolated perfused guinea-pig hearts. The following resulted were noted. (1) Calcium-dependent exocytotic NE release evoked by electrical field stimulation (12 Hz, 1 min) was completely suppressed after only 3 min of normothermic (37.5 degrees C) Bretschneider's cardioplegia. (2) Stop-flow ischemia is associated with a substantial calcium-independent, non-exocytotic NE release, which is regarded as a sodium-dependent carrier-mediated process. Accordingly, it is inhibited by blockers of the sodium/proton-exchanger (e.g. amiloride) and the neuronal uptake1-carrier (e.g. desipramine). Compared with stop-flow ischemia alone, cardioplegia with 3 min of Bretschneider's histidine-tryptophan-ketoglutarate (HTK)-solution preceding stop-flow enhanced NE release at all stop-flow durations (10-90 min) investigated (e.g. after 30 min of normothermic Bretschneider's cardioplegia: 1070+/-41 pmol/g, n = 45, v stop-flow alone: 764+/-48 pmol/g, n = 27, P<0.05). The NE concentrations determined in the cardiac effluent upon reperfusion followed a typical first order kinetic indicating that the transmitter release had already occurred during stop-flow. Hypothermia reduced NE release in a temperature-dependent manner down to intramyocardial temperatures of 2 7.5 degrees C. NE release evoked by Bretschneider's cardioplegia still exceeded that induced by stop-flow ischemia alone by up to 60%. The NE release evoked by Bretschneider's cardioplegia and stop-flow ischemia was calcium-independent. However, it was significantly reduced by desipramine and amiloride, but both agents had a more pronounced inhibitory effect on NE release evoked by stop-flow ischemia alone. (3) This difference may be due to an intrinsic effect of Bretschneider's HTK-solution, as continuous administration of normothermic Bretschneider's HTK-solution induced a substantial NE release which was neither calcium-dependent nor inhibited by blockade of either uptake1 or sodium/proton-exchange. It is concluded that Bretschneider's cardioplegia is not neuroprotective, as it even augments the stop-flow ischemia-induced nonexocytotic NE release.

Adrenergic Uptake Inhibitors↗
PubMed1999

Angiotensin inhibition and atrial natriuretic peptide release after acute volume expansion in rats with aortocaval shunt.

OBJECTIVE: In heart failure atrial natriuretic peptide (ANP) release in response to volume expansion is impaired while the renin-angiotensin system is activated. This study was designed to test the hypothesis that ANP release in heart failure is dependent on an activated angiotensin system. METHODS: We studied the ANP and renin-angiotensin systems in a rat model of shunt-induced high-output heart failure, in which we rapidly increased circulating fluid volume with a 5 ml, hyperoncotic infusion, and evaluated the effects of acute inhibition of the angiotensin converting enzyme as well as of the blockade of the angiotensin II type 1 receptors on the ANP release and on renal excretory function. RESULTS: ANP and angiotensin II plasma concentrations prior to volume expansion were elevated (p < 0.05) in rats with aortocaval shunt compared to controls. The diuretic response to acute volume expansion (18.5 +/- 1.5 vs. 48.2 +/- 2.4 microliters/min, p < 0.001) was markedly blunted. ANP release was attenuated in rats with aortocaval shunt, as was the increase of its second messenger cGMP in plasma and urine. The blunted increase in ANP plasma levels was not due to depleted cardiac stores as cardiac ANP content, as well as ANP synthesis, were increased (p < 0.05). Acute inhibition of the angiotensin converting enzyme as well as blockade of the angiotensin II type 1 receptors restored ANP release in response to volume expansion (p < 0.01). Moreover, acute inhibition of the renin-angiotensin system completely normalized the diuretic response. CONCLUSIONS: Our data suggest that the ANP system is impaired in rats with aortocaval shunt. The activation of the angiotensin system contributes to the impairment of the ANP system. Acute inhibition of the angiotensin II system significantly improved the ability of the ANP system to respond to acute volume expansion. Our findings indicate a hitherto fore unappreciated interaction between both systems and suggest additional mechanisms for the beneficial effects of angiotensin converting enzyme inhibition or angiotensin II type 1 receptor antagonists in heart failure.

Angiotensin II↗
PubMed1999

Desensitization of the pulmonary adenylyl cyclase system: a cause of airway hyperresponsiveness in congestive heart failure?

OBJECTIVES: This study was designed to investigate whether the adrenergic signal transduction in the lung and the responsiveness of airway smooth muscle to adrenergic stimulation are modulated in congestive heart failure. BACKGROUND: Wheezing and airway hyperresponsiveness are often present in heart failure. In the failing heart, chronic adrenergic stimulation down-regulates beta-adrenergic receptors and adenylyl cyclase. We hypothesized that airway dysfunction in heart failure could be due to a similar modulation of pulmonary adrenergic signal transduction. METHODS: Heart failure was induced in rats by aortic banding, resulting in increases in plasma norepinephrine, lung wet weight indicating congestion and left ventricular end diastolic pressure after four weeks. Beta-receptor densities in pulmonary plasma membranes were measured by radioligand binding using [125I]iodocyanopindolol. The G protein levels were determined by Western blot. Adenylyl cyclase activities in lung membranes were quantified as [32P]cAMP (cyclic adenosine-5'-monophosphate) synthesis rate. To functionally assess airway smooth muscle relaxation, carbachol-precontracted isolated tracheal strips were used. RESULTS: Beta-receptor density was significantly decreased in heart failure from 771 +/- 89 to 539 +/- 44 fmol/mg protein without changes in receptor affinities. The beta1-/beta2-subtype ratio, however, remained constant. The G(i and alpha) and G(s alpha) protein expression was unchanged. Adenylyl cyclase activity stimulated directly with forskolin was decreased by 28%. Relaxation of tracheal strips in response to isoproterenol and forskolin, but not to papaverin, was diminished by 30%. CONCLUSIONS: In heart failure, the down-regulation of pulmonary beta-receptors and concomitant decrease in adenylyl cyclase activity result in a significant attenuation of cAMP-mediated airway relaxation. These mechanisms may play a pivotal role in the pathogenesis of"cardiac asthma."

Adenylyl Cyclases↗
PubMed1998

Effect of moxonidine on blood pressure and sympathetic tone in conscious spontaneously hypertensive rats.

The effects of moxonidine on blood pressure, heart rate and sympathetic tone were studied in conscious spontaneously hypertensive rats. Intravenous moxonidine (80 nmol) transiently increased blood pressure without affecting heart rate or splanchnic nerve activity. Moxonidine (20-80 nmol) given into the fourth cerebral ventricle dose-dependently lowered mean arterial pressure, heart rate and sympathetic outflow (maximally by 60 +/- 3 mm Hg, 148 +/- 10 beats min(-1) and 15 +/- 3 microV). Moxonidine was more effective by this route than after the injection into the lateral ventricle. Clonidine (20-80 nmol) produced an initial pressor response after both intracerebroventricular routes of administration. A decrease in blood pressure was observed only when clonidine was given into the fourth ventricle. Clonidine decreased heart rate and splanchnic nerve activity similarly like moxonidine when the substances were given into the fourth ventricle. The data imply that the hypotensive effect of moxonidine is related to central sympathoinhibition. The main site of this action appears to be in the brainstem region.

Animals↗
PubMed1997

Dual effect of digitalis glycosides on norepinephrine release from human atrial tissue and bovine adrenal chromaffin cells: differential dependence on [Na+]i and [Ca2+]i.

It was the aim of the present study (1) to characterize the influence of Na+/K(+)-ATPase inhibition by the digitalis glycoside ouabain on both spontaneous and nicotine-evoked norepinephrine release from the human heart; and (2) to further investigate the role of glycoside-induced changes in [Na+]i and [Ca2+]i (determined by microfluorimetry) for catecholamine release. The latter experiments were performed in bovine adrenal medullary chromaffin cells (BCC), an established cell culture model for sympathetic nerves. Ouabain (1-1000 mumol/l) exerted a dual effect on norepinephrine release (determined by HPLC) from incubated human atrial tissue: (I) Ouabain induced a concentration-dependent increase in norepinephrine release, that was calcium-independent and almost completely prevented by blockade of the uptake1-carrier by desipramine (1 mumol/l). The characteristics of this release process are consistent with a non-exocytotic mechanism. (II) In addition, ouabain augmented the nicotine-evoked (1-100 mumol/l) calcium-dependent norepinephrine release, which can be considered to be exocytotic. Na+/K(+)-ATPase inhibition also reduced the threshold concentration of nicotine from 10 to 1 mumol/l and it delayed the rapid tachyphylaxis of its norepinephrine releasing effect in human atrial tissue. In BCC, ouabain increased [Na+]i, [Ca2+]i and [3H]-norepinephrine release in parallel. Under calcium-free conditions, not only the ouabain-induced increase in [Na+]i, but also [3H]-norepinephrine release were enhanced. The ouabain-induced [3H]-norepinephrine release was always closely related to changes in [Na+]i, indicating a key role of [Na+]i for this calcium-independent non-exocytotic norepinephrine release. In addition, pretreatment with ouabain (1 mmol/l) augmented the nicotine-evoked (0.1-10 mumol/l) increments in [Na+]i, [Ca2+]i and [3H]-norepinephrine release. As nicotine-induced norepinephrine release depends on an increase in both [Na+]i and [Ca2+]i, these findings are indicative of an ouabain-mediated facilitation of exocytosis. In conclusion, increasing [Na+]i and [Ca2+]i inhibition of Na+/K(+)-ATPase by ouabain triggers non-exocytotic norepinephrine release, and facilitates nicotine-evoked exocytotic norepinephrine release.

Adrenal Medulla↗
PubMed1997

Nicotine and sympathetic neurotransmission.

Nicotine increases heart rate, myocardial contractility, and blood pressure. These nicotine-induced cardiovascular effects are mainly due to stimulation of sympathetic neurotransmission, as nicotine stimulates catecholamine release by an activation of nicotine acetylcholine receptors localized on peripheral postganglionic sympathetic nerve endings and the adrenal medulla. The nicotinic acetylcholine receptor is a ligand-gated cation channel with a pentameric structure and a central pore with a cation gate, which is essential for ion selectivity and permeability. Binding of nicotine to its extracellular binding site leads to a conformational change of the central pore, which results in the influx of sodium and calcium ions. The resulting depolarization of the sympathetic nerve ending stimulates calcium influx through voltage-dependent N-type calcium channels, which triggers the nicotine-evoked exocytotic catecholamine release. In the isolated perfused guinea-pig heart, cardiac energy depletion sensitizes cardiac sympathetic nerves to the norepinephrine-releasing effect of nicotine, as indicated by a leftward shift of the concentration-response curve, a potentiation of maximum transmitter release, and a delay of the tachyphylaxis of nicotine-evoked catecholamine release. This sensitization was also shown to occur in the human heart under in vitro conditions. Through the intracardiac release of norepinephrine, nicotine induces a beta-adrenoceptor-mediated increase in heart rate and contractility, and an alpha-adrenoceptor-mediated increase in coronary vasomotor tone. The resulting simultaneous increase in oxygen demand and coronary resistance has a detrimental effect on the oxygen balance of the heart, especially in patients with coronary artery disease. Sensitization of the ischemic heart to the norepinephrine-releasing effect of nicotine may be a trigger for acute cardiovascular events in humans, such as acute myocardial infarction and/or life-threatening ventricular tachyarrhythmias.

Animals↗
PubMed1997

Ventricular arrhythmias in dilated cardiomyopathy.

Although prognosis of dilated cardiomyopathy (DCM) has improved due to advances in diagnosis and therapy, still too many sudden cardiac deaths occur in DCM. Spontaneous ventricular ectopy is a very common finding in patients with DCM, but the prognostic significance of Holter monitoring remains controversial. Other noninvasive methods, e.g., late potentials and QT dispersion, have not yet contributed to the evaluation of prognosis for arrhythmogenic events in DCM. Programmed ventricular stimulation has been repeatedly used to stratify long-term prognosis, yet satisfactory data are still missing as many deaths occur in patients without inducible arrhythmias. Several prognostic studies are still in progress, and preliminary data for the use of ICDs already appear to be promising. In patients with poor left ventricular function and ICDs in situ, prognosis is determined by progression of heart failure. Heart transplantation may be the ultimate therapeutic instrument for end-stage heart failure patients. For patients with advanced DCM and increased risk for malignant arrhythmias who are unsuitable for orthotopic heart transplantation, the combined therapy with an ICD and dynamic cardiomyoplasty may be an alternative treatment.

Arrhythmias, Cardiac↗
PubMed1997

Baroreflex sensitivity and heart rate variability in conscious rats with myocardial infarction.

The baroreflex sensitivity (BRS) and the heart rate variability (HRV) were studied in conscious rats after myocardial infarction (MI; induced by coronary artery ligation) and after sham operation (SH). BRS was determined by linear regression of R-R interval vs. arterial pressure changes induced by nitroprusside or methoxamine (intravenous bolus). HRV was calculated from 3-min electrocardiogram recordings. Left ventricular end-diastolic pressure and plasma atrial natriuretic peptide were increased after MI; plasma norepinephrine and basal heart rate (HR) remained unchanged. At 3 and 28 days after MI, BRS was reduced as indicated by decreased reflex bradycardia (RB) (MI, 0.66 +/- 0.13 and 0.78 +/- 0.07 ms/mmHg; SH, 1.27 +/- 0.16 and 1.48 +/- 0.14 ms/mmHg, respectively; P < 0.05 MI vs. SH). At 56 days after MI, BRS was normalized. RB was unaffected by atropine 3 and 28 days after MI but reduced in all other groups. The increase of basal HR by atropine 3 and 28 days after MI was less than in all other groups. HRV (SD of mean N-N interval, coefficient of variance, low- and high-frequency power; studied at 28 and 56 days) was similar in all groups. It is concluded that BRS is transiently depressed in rats with left ventricular dysfunction after MI probably due to a reduced reflex vagal activity. Even though basal HR and HRV are unchanged after MI, a temporary attenuation of tonic vagal activity is unmasked after autonomic blockade.

Analysis of Variance↗