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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Holter recordings of subjects apparently free from cardiovascular disease have demonstrated a moderate sinusal and nodal depression during sleep. This depression does not seem to be sufficient to create overt cardiovascular disorders in apparently healthy subjects, but it may aggravate or even reveal an underlying disorder of rhythm or conduction in elderly people or in patients taking drugs that potentiate its effects. In sleep apnea syndrome prolonged episodes of apnea may produce a paroxysmal, then permanent increase in pulmonary arterial pressure, which may lead to right heart failure. These episodes also increase the pre- and after-load and decrease myocardial contractility, thus facilitating the occurrence of left ventricular failure, potentiated by systemic arterial hypertension, overweight or even coronary disease, all conditions that are often present in these subjects. Arterial hypertension is so frequent in sleep apnea syndrome that some authors advocate a systematic search for the syndrome by Holter recordings before the hypertension is pronounced "essential". All studies confirm the existence of rhythm and conduction disorders directly related to apneic episodes. These disorders decrease or regress after a well-conducted treatment of the sleep apnea syndrome. They are mainly of the "hypokinetic" type, created by depression of sinus activity and conduction pathways. Their frequency, their severity and, in particular, the risk of sudden death they carry seem to have been overestimated, especially since no evidence has ever been produced of a potentially lethal rhythm disorder occurring during sleep apnea. Nevertheless, there is no certainty that these patients are not at risk of sudden death related to their sleep apnea syndrome.
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PMID:[Cardiovascular disorders during sleep]. 214 78

We report herein, a patient with a rectal carcinoid tumor of less than 1 cm in diameter with lymph node metastasis, and discuss a surgical policy for these lesions with reference to other such cases reported in the literature. A 40 year old female was admitted with a rectal mass and colonoscopy revealed a subpedunculated lesion, 1 cm in diameter, with a depression in its tip. A diagnosis of carcinoid was made by biopsy and transsacral excision performed. The excised specimen revealed a subpedunculated lesion measuring 7 X 6 X 6 mm with a central depression. The tumor was histologically confined to the submucosa but lymphatic invasion with pararectal lymph node involvement was observed. A radical proctectomy was thus performed. The incidence of metastasis from rectal carcinoids with a diameter of 1 cm or less is very low ranging from 1.5 to 3.4 per cent, and it therefore seems that most lesions of 1 cm or less in diameter can be treated by local excision alone. Thus, although it is recommended that local excision be performed first to determine the extent of spread, lymphatic vessel invasion and lymph node metastasis, radical surgery is indicated if lymphatic invasion or nodal involvement is present, even when muscle invasion is absent.
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PMID:A rectal carcinoid tumor of less than 1 cm in diameter with lymph node metastasis: a case report and a review of the literature. 220 13

To evaluate the clinical significance of ST segment depression observed during paroxysmal supraventricular tachycardia, the data of 100 patients who underwent electrophysiologic testing between 1981 and 1986 in the drug free state were reviewed. Twelve lead electrocardiograms were taken within 20 s of tachycardia induction. Patients with antidromic tachycardia, tachycardia using multiple accessory pathways or tachycardia associated with bundle branch aberration or concomitant electrolyte abnormalities were excluded from the study. Significant ST depression was defined as at least 0.1 mV horizontal or downsloping or 0.2 mV upsloping depression, measured 80 ms after the J point. ST segment changes were correlated with historical data and the results of exercise tests and radionuclide or coronary angiograms. There were 52 males and 48 females, aged 11 to 67 years (mean 32.8 +/- 13.2). Tachycardia was due to atrioventricular reentry via an overt or concealed accessory pathway in 85 patients, and atrioventricular nodal reentry in 15 patients. Significant ST depression was seen in 51 patients (aged 11 to 65 years). Thirty-three of 70 patients younger than 40 years old had significant ST depression. There was no relationship between the presence of significant ST depression and age, sex, mechanism or rate of tachycardia. Only three patients had significant coronary artery disease, and all manifested significant ST depression during tachycardia. Thus the specificity of this finding was 51% and the predictive value only 6%. In conclusion, ST segment changes observed during narrow QRS complex tachycardia are common, nonspecific and a poor predictor of underlying coronary artery disease.
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PMID:Incidence and clinical significance of ST segment depression in supraventricular tachycardia. 226 94

The purpose of this study was to determine if the known frequency-dependent effects of diltiazem on inward calcium current result in selective actions during supraventricular tachycardia. These effects were evaluated by use of an experimental model of orthodromic atrioventricular reentrant tachycardia (AVRT). AVRT was induced in 15 dogs over a wide range of retrograde conduction times before and after two doses of diltiazem. Diltiazem produced a tachycardia-related suppression of atrioventricular nodal conduction resulting in greater efficacy for faster than for slower AVRTs. The degree of slowing for tachycardias that remained inducible after diltiazem administration was greater for AVRTs with a rapid initial rate (dose 1, 29%; dose 2, 40%) than for slower AVRTs (dose 1, 11%, p less than 0.01; dose 2, 18%, p less than 0.001). Rate-dependent AVRT slowing occurred because of a time-dependent phase of AH interval prolongation after the onset of tachycardia, which was observed only after diltiazem administration. to further clarify the mechanism of diltiazem's selective actions against faster tachycardias, its effects on the minimum pathway for reentry, or wavelength, were examined in four dogs. The ratio of refractory period to revolution time (RP/RT), an index of wavelength, was measured for each AVRT before and after diltiazem administration. Diltiazem increased the positive slope of the relation between RP/RT and the AVRT rate threefold compared with control (p less than 0.05). This rate-dependent effect prevented AVRT when RP/RT became greater than unity. In conclusion, rate-dependent atrioventricular node depression by diltiazem results in greater tachycardia slowing and higher rates of termination during atrioventricular reentrant tachycardias with faster initial rates and shorter retrograde conduction intervals.
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PMID:Antiarrhythmic actions of diltiazem during experimental atrioventricular reentrant tachycardias. Importance of use-dependent calcium channel-blocking properties. 229 37

The mechanisms responsible for slowing cardiac impulse conduction through the atrioventricular (AV) node are not well understood but include anatomical architecture, presence of cells with diverse electrophysiological characteristics, and modulation by autonomic nervous system. The present study was designed to determine the site of vagally induced slowing of conduction through the AV node. We attempted to correlate the electrophysiological response of AV nodal cells to postganglionic vagal stimulation applied in different regions of the node with the morphological findings and patterns of acetylcholinesterase-positive staining of nodal tissue. This multifaceted approach revealed that vagal stimulation produced localized hyperpolarization of the cells from the N region of the AV node, which correlated with the strong acetylcholinesterase positive staining of the central nodal area. In contrast, the density of the acetylcholinesterase staining decreased toward both the AN and His bundle regions, whereas vagal stimulation had a negligible effect on the cells from these regions. These results suggest that vagal-induced depression of AV nodal conduction is produced by release of acetylcholine predominantly around the midnodal region and the depressive action of acetylcholine is concentrated on the cells occupying the same region (i.e., the N cells). Thus, there appears to be a close juxtaposition of nerve elements and effector cells in the midnodal region of the AV node. This unique combination of available neuromediator and responding cells with hyperpolarization and depressed action potential determines the midnodal region as the focus of vagal effect on AV nodal conduction.
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PMID:Morphological and electrophysiological correlates of atrioventricular nodal response to increased vagal activity. 239 13

The efficacy of beta adrenergic blocking agents has been observed in the treatment of a variety of cardiac arrhythmias. Electrophysiological experiments demonstrated that beta receptor blocking drugs prevent catecholamine-induced alterations of the transmembrane action potential. Clinically used beta blocking agents are effective in preventing arrhythmias provoked by sympathetic stimulation such as sinus tachycardia, paroxysmal junctional tachycardia, atrial, nodal, and ventricular premature contractions. Beta receptor blocking drugs are especially useful in tachycardias based on hyperkinetic heart syndrome and in exercise-induced premature beats in patients suffering from coronary heart disease. Beta blocking agents are--at least in our hands--most useful in combination with class I antiarrhythmic drugs with the intention to reduce the dosage--i.e. the side effects--of various antiarrhythmic drugs. In hyperthyroidism beta adrenergic blocking agents are effective complementary to the specific treatment. In cases of intoxication with beta blocking drugs complicated by myocardial depression and severe bradycardia glucagon must be regarded as a very useful compound.
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PMID:[Spectrum of effects of beta receptor blockade in cardiac arrhythmias]. 243 70

The acute electrophysiologic effects of 10 mg bisoprolol (B, given intravenously) were evaluated during an electrophysiological study in 10 patients with a history of paroxysmal tachycardia. Drug administration resulted in a significant decrease of sinus rate (Control [C]; 70.8/min; B: 59.4), and in an increase in sinus node recovery time (+20%). AV-nodal depression was marked at high heart rates during incremental atrial pacing. A second-degree AV-block occurred at a pacing cycle length (CL) of 329 ms (182/min) before and at a CL of 378 ms (158/min) after drug administration. Depression of AV-nodal conduction was negligible at low heart rates; the AH-interval at sinus rhythm was not affected (C: 84 ms, B: 86 ms); and functional and effective refractory periods of the AV-node were only slightly prolonged. Conduction intervals and refractory periods on atrial and ventricular level did not change. In 5 of 6 patients with accessory AV-pathways, circus movement tachycardia (CMT) could be elicited prior to as well as after B. Due to AV-nodal delay, CMT CL was slightly prolonged after B. Echozone and refractoriness of accessory pathways were not affected. In 1 of 2 patients with ectopic atrial tachycardia, B prevented the induction of paroxysms. In one patient with paroxysmal atrial fibrillation, the ventricular response decreased from 128/min to 94/min. The findings suggest that the electrophysiologic effects of B are due to a selective beta-adrenergic antagonism. Therapeutic efficacy is only to be expected if an increased adrenergic drive is a prerequisite for induction and continuation of a tachycardia.
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PMID:Electrophysiologic effects of an acute beta-blockade induced by bisoprolol in patients with supraventricular tachycardia as assessed by His-bundle electrograms. 243 91

The relationships between plasma drug concentrations and cardiovascular effects during combined administration of nifedipine and propranolol were evaluated in dogs anesthetized with thiopental. Three received small intravenous (i.v.) doses of nifedipine followed by propranolol, and 6 were given higher doses of nifedipine followed by propranolol; in 5, the order of drug doses was reversed, with propranolol administration followed by nifedipine. When dosing regimens that produced stable plasma levels of both drugs were used, the observed effects were closely related to the plasma concentrations of the individual agents. When small doses of nifedipine were combined with propranolol, at plasma levels associated with a significant degree of beta-adrenoceptor blockade, moderate decreases in spontaneous heart rate and cardiac output as well as increases in atrioventricular conduction time were produced. With higher doses of nifedipine, combined infusion with propranolol resulted in more pronounced depression in cardiac function, characterized by decreases in cardiac output, heart rate, and mean pulmonary arterial pressure, as well as increases in atrioventricular conduction time. When propranolol administration was followed by nifedipine, similar dose-dependent cardiovascular effects resulted, with profound toxicity apparent when large doses of nifedipine were used. These studies in an acute anesthetized dog model suggest that the magnitude of cardiovascular depression resulting from nifedipine and propranolol in combination is dependent on the plasma concentrations of both agents. Furthermore, in the presence of beta-adrenoceptor blockade, the direct effects of nifedipine on myocardial conducting tissue, which are usually absent when this calcium antagonist is given alone, may become apparent and result in depression of atrioventricular and sinoatrial nodal functions.
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PMID:Nifedipine-propranolol interaction: dependence of cardiovascular effects on plasma drug concentrations. 244 Nov 69

1. The nature, distribution and function of rectifying channels in rat spinal root myelinated axons has been assessed with selective blocking agents and a variety of intracellular and extracellular recording techniques. 2. The electrotonic responses of roots poisoned with tetrodotoxin (TTX) to constant current pulses had fast (rise time much less than 1 ms) and slow components, which were interpreted in terms of Barrett & Barrett's (1982) revised cable model for myelinated nerve. Depolarization evoked a rapid outward rectification (time constant, tau approximately 0.5 ms), selectively blocked by 4-aminopyridine (4AP, 1 mM), and a slow outward rectification (tau approximately 15 ms), selectively blocked by tetraethylammonium (TEA, 1 mM) or Ba2+ (0.5 mM). Hyperpolarization evoked an even slower inward rectification, selectively blocked by Cs+ (3 mM) but not by Ba2+. 3. From the different effects of the blocking agents on the fast and slow components of electrotonus, it was deduced (a) that the inward rectification is a property of the internodal axon, (b) that the slow outward rectifier is present at the nodes, and probably the internodes as well, and (c) that the 4AP-sensitive channels have a minor nodal and a major internodal representation. 4. TEA and Ba2+ reduced the accommodation of roots and fibres not poisoned with TTX to long current pulses, whereas 4AP facilitated short bursts of impulses in response to a single brief stimulus. 5. TEA and Ba2+ also abolished a late hyperpolarizing after-potential (peaking at 20-80 ms), while 4AP enhanced the depolarizing after-potential in normal fibres, and abolished an early hyperpolarizing after-potential (peaking at 1-3 ms) in depolarized fibres. Corresponding to the later after-potentials were post-spike changes in excitability and conduction velocity, which were affected similarly by the blocking agents. Cs+ increased the post-tetanic depression attributable to electrogenic hyperpolarization. 6. The physiological roles of the three different rectifying conductances are discussed. It is also argued that the prominent ohmic 'leak conductance', usually ascribed to the nodal axon, must arise in an extracellular pathway in series with the rectifying internodal axon.
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PMID:Function and distribution of three types of rectifying channel in rat spinal root myelinated axons. 244 52

Previous studies suggest that high levels of adenosine may enhance histamine release and contribute to atrioventricular (AV) nodal conduction arrhythmias during anaphylaxis of isolated guinea pig hearts. To determine whether elevations in endogenous adenosine evoked by hypoxic conditions have similar effects, isolated hearts of guinea pigs passively sensitized by intracardiac injection were perfused with solutions equilibrated with 95% O2 (normoxia) or 30% O2 (hypoxia). When compared with normoxia, hypoxia before antigen challenge increased adenosine release, decreased vascular resistance, and prolonged P-R intervals, whereas hypoxia during anaphylaxis potentiated the increase in adenosine release, attenuated the increases in vascular resistance and atrial rate, and increased the occurrence of conduction arrhythmias without altering the antigen-induced release of either histamine or thromboxane. Addition of the adenosine receptor antagonist 8-(4-sulfophenyl)theophylline (SP-T) to the hypoxic perfusate significantly decreased antigen-induced release of histamine and thromboxane. These data indicate that 1) hypoxia-induced depression of antigen-induced mediator release may be counteracted by the stimulatory effect of the increased adenosine induced by hypoxia, and 2) under hypoxic conditions, adenosine's negative dromotropic, chronotropic, and vasodilatory effects may influence the anaphylactic reaction.
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PMID:Role of adenosine in hypoxic alterations of anaphylaxis of isolated guinea pig hearts. 258 93


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