Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

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

Split-dose thallium-dipyridamole myocardial scintigraphy was performed in patients with nonobstructive hypertrophic cardiomyopathy (HC) who had angiographically normal coronary arteries. The dipyridamole-induced increases in thallium-201 uptake, calculated to evaluate coronary vasodilatory capacity, were significantly lower in 30 patients with HC than in 13 control subjects (177 +/- 58 vs 281 +/- 46%) and the reductions were observed in both the septal and lateral segments. The reductions of the septal segment in HC patients were significantly greater than those in 10 hypertensive patients with comparable degrees of septal hypertrophy. Of patients with HC, 16 had increases in thallium uptake well below the normal range. Compared with those having normal increases, these patients had significantly lower exercise duration (11 vs 15 minutes), with 33% having ST depression develop at a workload less than or equal to 80 watts. These data indicate that approximately one-half of patients with HC have impaired coronary vasodilatory capacity that could be an important pathophysiologic abnormality of HC resulting in the development of myocardial ischemia and the impairment of cardiac performance during exercise.
...
PMID:Decreased coronary vasodilatory capacity in hypertrophic cardiomyopathy determined by split-dose thallium-dipyridamole myocardial scintigraphy. 233 Sep

Verapamil is used clinically in the treatment of various cardiac diseases including hypertrophic cardiomyopathy. Its long term effects on ventricular mass are not well known. In 11 conscious dogs heart rate, aortic and left ventricular pressures, cardiac output, a methoxamine induced stress ventricular function test and left ventriculography were performed. These variables were measured prior to and following a mean 7.2 month infusion of verapamil at 0.005 or 0.01 mg.kg-1.min-1 using a subcutaneously implanted pump. Resting haemodynamic variables and left ventricular ejection fraction [60(SD 6) v 55(6)%] were unchanged between baseline and chronic verapamil studies, but the slope of the methoxamine induced stress ventricular function test decreased from 3.9(0.8) to 2.1 (1.3). After verapamil was discontinued the mean slope of the stress ventricular function test returned to the baseline 4.0(1.7). Total ventricular weight increased 22% from 176.1(17.5) g.m-2 in controls to 215.6(29.5) g.m-2 (p less than 0.01) in the verapamil animals. The right ventricular weight increased 25% from 46(5.9) to 57.6(9.1) g.m-2 (p less than 0.01); the septum weight increased 26% from 42.5(4.1) to 53.7(7.2) g.m-2 (p less than 0.001); and the left ventricular free wall weight increased 19% from 87.4(9.8) to 103.9(15.7) g.m-2 (p less than 0.01). The increase in ventricular weights was not due to fibrosis or oedema since hydroxyproline contents and wet/dry ratios were not increased. In conclusion, a chronic infusion of verapamil in conscious dogs caused no change in resting haemodynamic variables but produced reversible depression of stress ventricular function and biventricular and septal hypertrophy.
...
PMID:Verapamil induced ventricular hypertrophy in conscious dogs. 253 64

In experimental studies, minute sinusoidal vibration has been reported to induce functional depression of the left ventricle and to be an index for evaluation of myocardial crossbridge kinetics. Therefore, to examine whether or not this vibration-induced functional depression could also be observed in the human ventricle, motion of the left ventricular (LV) wall or LV pressure was measured by echocardiography (n = 16) or by left heart catheterization (n = 4), in which 100 Hz, 2.07 mm-amplitude sinusoidal vibration was applied to the subject's precordium. In the echocardiographic study, left ventricular wall shortening did not change by vibration in nine healthy volunteers, but was depressed in two patients with aortic regurgitation (AR) and in one patient with ischemic heart disease (IHD). In measurement of LV pressure, the decrease in LV systolic pressure caused by vibration was obviously observed in two patients (AR and IHD) but was not observed in two patients with hypertrophic cardiomyopathy. These results suggest that we might be able to extend previously proposed experimental idea on early detection of the abnormality in myocardial crossbridge kinetics to the clinical setting.
...
PMID:Clinical demonstration of vibration-induced depression of left ventricular function. 262 67

The long-term prognosis for 314 patients with hypertrophic cardiomyopathy (HCM) and 82 with dilated cardiomyopathy (DCM) was investigated in an attempt to elucidate clinical variables predicting sudden death (SD). In the patients with HCM, 68% of cardiac deaths occurred suddenly and unexpectedly. Variables associated with an increased risk to SD were young age (less than 30 years), reduced fractional shortening (less than 35%) and elevated left ventricular end-diastolic pressure (greater than or equal to 20 mmHg). Eight of the 10 patients who died suddenly during or immediately after strenuous exercise were less than 30 years old, and the collapse tended to be associated with exercise-induced ST-depression. In contrast, SD occurring during mild activities, resting or sleep was mainly observed in those aged 30 years or more. Ventricular tachycardia was observed on electrocardiographic monitoring in 24% of those 30 years or more, while it was rare in those under 30 years (5%). On the other hand, no SD was found in patients with apical hypertrophy nor in those 50 years or more. These observations suggest that HCM patients at a young age, with impaired left ventricular systolic and diastolic function, have an increased risk to SD. Since exercise-induced myocardial ischemia rather than ventricular arrhythmias appears to be the more likely mechanism for SD for those under 30 years old, restriction of strenuous exercise should be strongly advised for these patients. For those aged from 30 to 50 years, ventricular tachycardia should be controlled by antiarrhythmic agents for the prevention of SD. In patients with DCM, 24% of all cardiac deaths were attributed to SD. Although no variables reliably predicted SD, it was of note that only one patient out of 26 with SV1 + RV5 greater than or equal to 35 mm died suddenly. Whereas ventricular arrhythmias are known to be a contributing cause for SD, the prognostic significance of ventricular tachycardia on electrocardiographic monitoring in predicting SD has not yet been established. In addition, antiarrhythmic agents often precipitate hemodynamic deterioration. It therefore appears that use of antiarrhythmic agents is not a therapy of first choice and that primary treatment should be focused upon improvement in ventricular function in order to prevent SD in patients with DCM.
...
PMID:Sudden death in hypertrophic and dilated cardiomyopathy. 263 25

To study the clinical significance of abnormal myocardial perfusion in patients with hypertrophic cardiomyopathy (HCM), we performed a computerized washout analysis of digital subtraction coronary arteriograms in 28 patients with HCM and 16 control subjects. The contrast disappearance half-life (T1/2) was calculated from a time-density curve generated in the four sectors of the myocardium perfused by the left anterior descending coronary artery and the mean T1/2 was calculated by averaging T1/2 values for these four sectors. Patients with HCM demonstrated longer T1/2 in the ventricular septal region than control subjects. Thirteen (46%) of the patients with HCM presented abnormally longer mean T1/2 values, suggesting impaired myocardial perfusion. Family histories of HCM were more frequent in patients with abnormal mean T1/2 values (92% vs 47%; p less than 0.05). On the exercise stress test, patients with abnormal T1/2 values presented significantly lower exercise tolerance with more frequent exercise-induced ST segment depression (62% vs 13%; p less than 0.05). However, there were no significant differences between the two groups with regard to ventricular wall thickness, left ventricular end-diastolic pressure, or the severity of systolic narrowing of the coronary arteries. These findings suggest that 13 (46%) of the patients with HCM have impaired myocardial perfusion, which may be a manifestation of intramural coronary artery disease in addition to left ventricular hypertrophy, elevated left ventricular end-diastolic pressure, or systolic narrowing of the coronary arteries. Additionally, significant association of the prolonged T1/2 with a familial occurrence of HCM and depressed exercise tolerance with ST segment depression imply that impaired myocardial perfusion could be an important inherent pathophysiological state leading to myocardial ischemia during exercise.
...
PMID:Impaired myocardial perfusion in patients with hypertrophic cardiomyopathy: assessment with digital subtraction coronary arteriography. 297 83

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

Prevention of sudden arrhythmic cardiac death must be preceded by identification of the high-risk patient to whom appropriate therapy can be given. The most common disease state associated with sudden cardiac death is coronary artery disease. Factors which identify a high-risk subset include: left ventricular dysfunction; frequent and complex arrhythmias on Holter monitoring; abnormal signal-averaged electrocardiograms; angina, ST depression, and exertional hypotension or ventricular arrthythmias on exercise testing; inducible sustained arrhythmias at electrophysiologic testing, or a combination of these factors. Other conditions which are known to be associated with sudden death include: dilated or congestive cardiomyopathy, hypertrophic cardiomyopathy, mitral valve prolapse, valvular heart disease, Wolff-Parkinson-White syndrome, myocarditis, congenital heart disease, electrolyte abnormalities, long QT syndromes, proarrhythmic effects of drugs, and less common conditions such as myocardial tumors and pulmonary hypertension. If the primary abnormality responsible for the tendency toward arrhythmias cannot be corrected, appropriate therapy should be administered to attempt to reduce the patient's risk of sudden arrhythmic cardiac death.
...
PMID:Definition of patients at high risk of sudden arrhythmic cardiac death. 327 Nov 94

The haemodynamic effects of an intravenous amiodarone infusion (5 mg/kg for 10 minutes) were measured in ten patients with hypertrophic cardiomyopathy (two with a left ventricular outflow gradient at rest) five, 15, and 30 minutes after drug administration. Mean (SD) pulmonary capillary wedge pressure rose significantly at five and 15 minutes (from 12.3 (6.2) mm Hg to 17.6 (9.2) and to 16.2 (8.6] with a subsequent tendency to fall to control values at 30 minutes. Mean right atrial and right ventricular end diastolic pressures increased from 3.6 (1.8) mm Hg to 7.3 (3.1) and from 6.3 (2.4) to 9.8 (3.2) mm Hg respectively at 30 minutes. The increase in filling pressures was paralleled by a decrease of left ventricular max dP/dt from 1522 (414) to 1372 (327) to 1316 (338) and to 1326 (379) five, 15, and 30 minutes after infusion. Despite this slight negative inotropic effect, cardiac index and stroke volume index were unchanged or slightly increased, possibly because of the decrease in systemic vascular resistance (from 1326 (330) dyn s cm-5/m2 to 1152 (285]. In both patients with outflow gradient the pressure gradient at rest decreased (from 110 to 65 and from 85 to 65 mm Hg) through a reduction of left ventricular systolic pressure. Thus short term intravenous infusion of amiodarone is safe in patients with hypertrophic cardiomyopathy. The main changes were a mild depression of ventricular contractility, which was well tolerated and adequately compensated for by a decrease in afterload.
...
PMID:Haemodynamic effects of short term intravenous amiodarone for hypertrophic cardiomyopathy. 337 Jan 79

The clinical profiles in patients with hypertrophic cardiomyopathy who had exercise-induced deterioration in systolic performance of the left ventricle (LV) were investigated using exercise echocardiography. The materials consisted of 32 patients, which who categorized in two groups according to the extent of % shortening fraction of the LV (% SF) at the peak exercise; 21 whose % SF was increased (group I: from 40.9 +/- 7.2% at rest to 44.2 +/- 8.0% at the peak exercise) and 11 whose % SF was decreased (group II: from 40.8 +/- 7.3% to 34.8 +/- 6.9%). There were no significant differences between these two groups as to the resting echocardiographic data or the prevalence of pressure gradient in the LV outflow tract. The frequency of symptoms, such as chest pain and exertional dyspnea, was higher in the group II (73%) than in the group I (38%). The time of exercise tolerance was significantly shorter in group II than in group I (I: 9.2 +/- 1.9 min., II: 7.4 +/- 2.6 min., p less than 0.05). Five patients (45%) in group II and four (19%) in group I developed at least 2 mm ST segment depression during exercise electrocardiography. Twenty-four hour ambulatory ECG monitoring showed a high prevalence of ventricular arrhythmias in group II. Seven (78%) of nine patients in group II and five (28%) of 18 in group I had abnormal 201T1 myocardial scintigrams. Left ventricular ejection fraction was not significantly different between the two groups, but the end-diastolic pressure was higher in group II (19 +/- 6 mmHg) than in group I (15 +/- 4 mmHg). All patients who underwent coronary arteriography had no significant stenosis. Thus, there are significant differences in the clinical features between the two groups of patients who had reciprocal LV responses during exercise. These findings should be considered in the management of patients with hypertrophic cardiomyopathy.
...
PMID:[Left ventricular systolic performance during exercise in patients with hypertrophic cardiomyopathy]. 365 13

In 14 patients with obstructive hypertrophic cardiomyopathy and angiographically normal coronary arteries, 8 with angina (group B) and 6 without (group A), the effects of intravenous isoproterenol, 2 to 4 micrograms/min, followed by intravenous propranolol, 0.2 mg/kg, were studied. An intraventricular systolic gradient less than 50 mm Hg, high-quality echocardiograms and cineangiograms and high-fidelity pressure tracings were selection criteria. Hemodynamic and metabolic variables were assessed during basal conditions, after 5 minutes of isoproterenol infusion or at angina and ST-segment depression, and 5 and 10 minutes after intravenous propranolol infusion. Isoproterenol increased the intraventricular systolic gradient more significantly in group B than in group A (102.4 +/- 8.3 vs 52.2 +/- 8.2, p less than 0.0001). Group B also had higher left ventricular end-diastolic pressure (32.5 +/- 3.9 vs 20.2 +/- 5.7), lower mean arterial pressure (69.7 +/- 3.5 vs 84.7 +/- 4.8) and a smaller increase in coronary sinus flow (176.1 +/- 9.2 vs 261.5 +/- 33.9, all p less than 0.0001), concomitant with lactate release and ST-segment depression. Propranolol promptly reversed hemodynamic and metabolic changes caused by isoproterenol, except for a further coronary sinus flow increase (from 176.1 +/- 9.2 to 219 +/- 14.2 ml/min, p less than 0.001), and heart rate decrease below basal values (57.8 +/- 7.5 vs 79.9 +/- 9.8 beats/min, p less than 0.001) in group B.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Mechanism of isoproterenol-induced angina pectoris in patients with obstructive hypertrophic cardiomyopathy and normal coronary arteries. 366 32


<< Previous 1 2 3 4 5 6 7 8 Next >>

---