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Lopressor (Metoprolol)

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Lopressor is a high-quality medication which is taken in treatment of high blood pressure. It also can be used in the treatment of chest pain, heart attacks.

Other names for this medication:
Dutoprol, Lopressor hct, Toprol-xl

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Also known as: Metoprolol.


Lopressor is a perfect remedy. Its target is to struggle against high blood pressure. It also can be used in the treatment of chest pain, heart attacks.

Lopressor acts by slowing the heart rate and relaxing the blood vessels. It is beta blocker.

Lopressor is also known as Toprol-XL, Metoprolol, Protomet, Lopresor, Lopresar.

Generic name of Lopressor is Metoprolol Tartrate.

Brand names of Lopressor are Toprol-XL, Lopressor.


Take Lopressor tablets orally with water.

Take Lopressor once or twice a day at the same time.

Do not crush or chew it.

If you want to achieve most effective results do not stop taking Lopressor suddenly.


If you overdose Lopressor and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Lopressor overdosage: fainting, difficulty, breathing or swallowing, swelling of the hands, feet, ankles, or lower legs, lightheadedness.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Lopressor are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Lopressor if you are allergic to Lopressor components.

Do not take Lopressor if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Lopressor if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Lopressor in case of taking cimetidine (Tagamet), clonidine (Catapres), diphenhydramine (Benadryl), fluoxetine (Prozac, Sarafem), hydroxychloroquine, paroxetine (Paxil), propafenone (Rythmol), quinidine (Quinaglute, Quinidex), ranitidine (Zantac), reserpine (Serpalan, Serpasil, Serpatab), ritonavir (Norvir), terbinafine (Lamisil),and thioridazine (Mellaril), bupropion (Wellbutrin).

Be careful with Lopressor if you have allergies to medicines, foods, or other substances.

Be careful with Lopressor if you suffer from or have a history of heart or liver disease; diabetes; severe allergies; or an overactive thyroid gland (hyperthyroidism), slow heart rate, heart failure, problems with blood circulation, or pheochromocytoma (a tumor that develops on a gland near the kidneys and may cause high blood pressure and fast heartbeat), had asthma or other lung disease.

Use Lopressor with great care in case you want to undergo an operation (dental or any other).

Avoid alcohol.

Avoid machine driving.

Do not stop taking Lopressor suddenly.

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In an attempt to resolve the controversy concerning use of beta-adrenoceptor blockade in patients undergoing coronary artery revascularization, 40 consecutive patients with ischaemic heart disease receiving chronic beta-adrenergic blocking therapy (study group) were entered into a randomized trial and were compared with 40 patients receiving no beta-blocking therapy (control group). The postoperative requirement for positive inotropic agents between the two groups was compared. The clinical and operative characteristics of the two groups were similar. After surgery, 2% of patients in the study group required positive inotropic agents compared with 18% of those in the control group (P < 0.05). It is concluded that this difference resulted from an increase in density of beta 1-adrenergic receptors induced by beta-adrenergic blockade, and an increase in the level of catecholamines in the early postoperative period.

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A kinetic spectrophotometric method has been described for the determination of metoprolol tartrate in pharmaceutical formulations. The method is based on reaction of the drug with alkaline potassium permanganate at 25+/-1 degrees C. The reaction is followed spectrophotometrically by measuring the change in absorbance at 610 nm as a function of time. The initial rate and fixed time (at 15.0 min) methods are utilized for constructing the calibration graphs to determine the concentration of the drug. Both the calibration graphs are linear in the concentration range of 1.46 x 10(-6)-8.76 x 10(-6) M (10.0-60.0 microg per 10 ml). The calibration data resulted in the linear regression equations of log (rate)=3.634+0.999 log C and A=6.300 x 10(-4)+6.491 x 10(-2) C for initial-rate and fixed time methods, respectively. The limits of quantitation for initial rate and fixed time methods are 0.04 and 0.10 microg ml(-1), respectively. The activation parameters such as E(a), DeltaH(double dagger), DeltaS(double dagger) and DeltaG(double dagger) are also evaluated for the reaction and found to be 90.73 kJ mol(-1), 88.20 kJ mol(-1), 84.54 J K(-1) mol(-1) and 63.01 kJ mol(-1), respectively. The results are validated statistically and through recovery studies. The method has been successfully applied to the determination of metoprolol tartrate in pharmaceutical formulations. Statistical comparison of the results with the reference method shows excellent agreement and indicates no significant difference in accuracy and precision.

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Identification of degradation products from trace organic compounds, which may retain the biological activity of the parent compound, is an important step in understanding the long-term effects of these compounds on the environment. Constructed wetlands have been successfully utilized to remove contaminants from wastewater effluent, including pharmacologically active compounds. However, relatively little is known about the transformation products formed during wetland treatment. In this study, three different wetland microcosm treatments were used to determine the biotransformation products of the β-adrenoreceptor antagonists atenolol, metoprolol and propranolol. LC/ESI-Q-ToF run in the MS(E) and MS/MS modes was used to identify and characterize the degradation products through the accurate masses of precursor and product ions. The results were compared with those of a reference standard when available. Several compounds not previously described as biotransformation products produced in wetlands were identified, including propranolol-O-sulfate, 1-naphthol and the human metabolite N-deaminated metoprolol. Transformation pathways were significantly affected by microcosm conditions and differed between compounds, despite the compounds' structural similarities. Altogether, a diverse range of transformation products in wetland microcosms were identified and elucidated using high resolving MS. This work shows that transformation products are not always easily predicted, nor formed via the same pathways even for structurally similar compounds.

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The efficacy of diltiazem in comparison with metoprolol in chronic stable angina was assessed in 33 male patients during a 15-week blind cross-over study. After an initial two-week run-in period, baseline measurements were made. Subsequently, the patients entered a blind cross-over study consisting of two six-week treatment periods with diltiazem 240 mg (60 mg q.i.d.) or metoprolol 200 mg (100 mg b.i.d.). Dose adjustment to either 360 mg diltiazem (120 t.i.d.) or 400 mg metoprolol (200 b.i.d.) was allowed two weeks after the start of treatment. There was a one-week washout period between the two treatment periods. Compared to baseline values both drugs reduced the number of anginal attacks (diltiazem - 55%, P = 0.02; metoprolol - 73%, P = 0.01) and showed improvement of the measured exercise variables (exercise duration: diltiazem + 16%, P less than 0.001; metoprolol + 4%, P = NS; time to angina: diltiazem + 21%, P = 0.02, metoprolol + 14%, P = NS; maximal ST-depression: diltiazem + 13%, P = NS, metoprolol + 33%, P = 0.002). No significant change in LVEF was noticed. Both drugs reduced the mean heart rate on Holter tape (diltiazem - 11%, P = 0.006; metoprolol - 14%, P = 0.004). No effects on conduction were noticed. Although at the borderline of significance, diltiazem increased the total exercise duration as compared to metoprolol (16 vs. 4%, P = 0.05). It is concluded that diltiazem improves exercise tolerance in patients with stable angina pectoris and appears to be a safe and effective alternative to the beta-blocking agent metoprolol.(ABSTRACT TRUNCATED AT 250 WORDS)

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This paper was designed to report the results of analysis of metoprolol succinate substance and tablets obtained from two manufacturers, Akrikhin (Russia) and AstraZeneca (Sweden). The analysis was performed by spectroscopy in the near IR region and followed by the chemometric treatment of the data obtained. The method was used to confirm the "identity" of metoprolol succinate tablets. The approach to distinguishing the differences between pharmaceutical dosage forms produced by different manufacturers is proposed. Also, the method for the qualitative determination of metoprolol succinate in the pharmaceutical formulations has been developed.

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A total of 29,357 antihypertensive patients were identified who initiated therapy with valsartan (n = 6,645), lisinopril (n = 17,320), or extended-release metoprolol (n = 5,392). In multivariate analyses, therapy with valsartan was associated with a significantly lower risk of a major cardiovascular or renal event versus extended-release metoprolol (heart rate [HR], 0.70; 95% confidence interval [CI], 0.56-0.87; p = 0.0015). Patients receiving valsartan had a nominally lower risk of a major cardiovascular or renal event than those receiving lisinopril, although this difference was not statistically significant (HR, 0.89; 95% CI, 0.74-1.07; p = 0.1987).

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Hemodynamic theories of atherogenesis suggest that flow disturbances (departures from laminar flow including high and low shear) and increases in heart rate may be important in the initiation, progression, and complications of atherosclerosis such as dissection and embolism. It is therefore desirable to evaluate the effects of antihypertensive drugs on the occurrence of such flow disturbances. Effects of metoprolol, nifedipine, and captopril were studied, by quantitative spectral analysis, in 20 patients with carotid stenosis to evaluate 3 indices of disturbed flow: peak velocity, spectral broadening index and window index (WI). Heart rate (HR), and the product of WI by HR, were improved (reduced) significantly by metoprolol (p < 0.05), and worsened by nifedipine (p < 0.05), but most of the effect was due to effects on heart rate. These findings suggest that most of the benefit of antihypertensive drugs on flow disturbances can be identified by counting heart rate. Further developments will require improved methods for quantitation of flow disturbances.

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The use of various doses of metoprolol (spesicor, Leiras, Finland), a selective beta 1-adrenoblocker, in patients with CHD combined with clinical or instrumentally detectable symptoms of bronchial asthma or stage I-II essential hypertension with angina pectoris of I-II functional classes, has shown that metoprolol cardioselective blockade is a relative phenomenon which has definite correlation with a dose, duration of therapy, and the initial status of the bronchopulmonary system. An antianginal effect was observed in 68.5% of patients, an antihypertensive effect--in 71.3%, side-effects--in 6.4%.

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Recent randomized clinical trials have shown that total mortality and cardiovascular mortality are reduced by the early intravenous administration of beta-blockers to patients suspected of suffering from acute myocardial infarction. These trials were conducted on patients meeting strict entry criteria. In order to assess this therapy when applied to a broader range of myocardial infarction patients, we performed a Phase IV study of metoprolol in acute myocardial infarction. The study was designed to test whether early (less than 8 hours from onset of chest pain) intervention by practicing physicians with open label intravenous metoprolol for cases of suspected acute myocardial infarction achieved mortality results similar to those obtained in large randomized clinical trials. We studied 3824 patients treated by 741 physicians representing a broad spectrum of clinical practice in the United States. Seventy-two percent of the patients entered into the study had confirmed myocardial infarction (39% anterior, 39% inferior, 22% other locations) and 85% of all individuals treated tolerated the full intravenous dose of 15 mg of metoprolol. The 15 day total mortality and cardiovascular mortality rates were 4.9% and 4.5%; 90 day mortality rates were 6.9 and 5.9%. Patients with anterior infarctions had a significantly greater cumulative mortality rate than patients with other types of infarctions. Marked bradycardia (heart rate less than 45 beats per minute) in the first 8 hours post treatment occurred in 4.7% cases and hypotension (systolic blood pressure less than 90 mm Hg) occurred in 9.8% of cases. When compared with the results of the Göteborg and MIAMI trials of metoprolol, it appears that there is no appreciable increase in mortality or morbidity when metoprolol is used in the community practice of acute coronary care.

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This case shows that percutaneous management without stenting coupled with aggressive anti-coagulation of cocaine induced coronary dissection may result in an acceptable outcome especially in a young otherwise fit and healthy patient.

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The latter half of the 1990s was a time of extraordinary progress in the understanding and management of atrial fibrillation (AF). Evidence that "AF begets AF" has generated considerable interest regarding the mechanisms responsible for this phenomenon and has sparked the development of new concepts in both pharmacologic and nonpharmacologic therapy. The recognition that, in some patients, AF is initiated and possibly maintained by atrial tachycardia originating in the pulmonary veins has challenged accepted notions regarding the mechanisms responsible for arrhythmia. New antiarrhythmic drugs, devices, ablation techniques, and pacing techniques have been developed and tested. Strategies for the use of existing therapies have been evaluated, and new indications for existing therapies are under consideration. This article reviews several studies published in 1999 and 2000 that addressed the mechanisms and the management of AF.

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In 1987, the Cardiac Arrest Study Hamburg (CASH), a prospective, multicenter, randomized controlled study, was started in survivors of sudden cardiac death resulting from documented ventricular tachyarrhythmias. Through December 1991, 230 survivors (46 women, 184 men; mean age 57 +/- 11 years) of cardiac arrest caused by ventricular tachyarrhythmias were randomly assigned to receive either oral propafenone (56 patients), amiodarone (56 patients), or metoprolol (59 patients) or to have an implantable defibrillator (59 patients) without concomitant antiarrhythmic drugs. The primary endpoint of the study was total mortality. In March 1992, the propafenone arm of CASH was stopped because of excess mortality compared with the implantable defibrillator group. This article presents preliminary results of the comparison of implantable defibrillator therapy with propafenone therapy. A significantly higher incidence of total mortality, sudden death (12%), and cardiac arrest recurrence or sudden death (23%) was found in the propafenone group compared with the implantable defibrillator-treated patients (0%, p < 0.05). It was concluded that, in survivors of cardiac arrest, propafenone treatment is less effective than implantable defibrillator treatment.

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Melanin-concentrating hormone (MCH) plays an important role in energy balance. The current studies were carried out on a new line of mice lacking the rodent MCH receptor (MCHR1(-/-) mice). These mice confirmed the previously reported lean phenotype characterized by increased energy expenditure and modestly increased caloric intake. Because MCH is expressed in the lateral hypothalamic area, which also has an important role in the regulation of the autonomic nervous system, heart rate and blood pressure were measured by a telemetric method to investigate whether the increased energy expenditure in these mice might be due to altered autonomic nervous system activity. Male MCHR1(-/-) mice demonstrated a significantly increased heart rate [24-h period: wild type 495 +/- 4 vs. MCHR1(-/-) 561 +/- 8 beats/min (P < 0.001); dark phase: wild type 506 +/- 8 vs. MCHR1(-/-) 582 +/- 9 beats/min (P < 0.001); light phase: wild type 484 +/- 13 vs. MCHR1(-/-) 539 +/- 9 beats/min (P < 0.005)] with no significant difference in mean arterial pressure [wild type 110 +/- 0.3 vs. MCHR1(-/-) 113 +/- 0.4 mmHg (P > 0.05)]. Locomotor activity and core body temperature were higher in the MCHR1(-/-) mice during the dark phase only and thus temporally dissociated from heart rate differences. On fasting, wild-type animals rapidly downregulated body temperature and heart rate. MCHR1(-/-) mice displayed a distinct delay in the onset of this downregulation. To investigate the mechanism underlying these differences, autonomic blockade experiments were carried out. Administration of the adrenergic antagonist metoprolol completely reversed the tachycardia seen in MCHR1(-/-) mice, suggesting an increased sympathetic tone.

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Antihypertensive medicines are to known to cause diverse disturbances to electrolyte homeostasis; however, their potential to affect zinc is less well known. The primary aim was to explore whether antihypertensive medicines have the potential to affect zinc status. Lipitor Prices

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Adults who initiated hypertension treatment with a beta blocker were identified from the MarketScan * claims database (2008-2012). Patients were classified based on their first beta blocker use: nebivolol, atenolol, carvedilol, metoprolol, and other beta blockers. Patients with compelling indications for atenolol, carvedilol Hyzaar Cost or metoprolol (acute coronary syndrome and congestive heart failure) were excluded. Patients enrolled in health maintenance organization or capitated point of service insurance plans were also excluded. Persistence was defined as continuous use of the index drug (<60 day gap). The average effect of persistence on medical costs (2012 USD) was estimated using generalized linear models (GLMs). Regression estimates were used to predict medical cost differences associated with persistence between nebivolol and the other cohorts.

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Thirteen patients meeting inclusionary criteria were enrolled. Therapeutic response was defined as conversion to sinus rhythm, a decline in the ventricular rate of 15 percent or more [corrected], or a ventricular rate of less than 100 beats/minute. Four male and nine female patients having a mean age (+/- SD) of 81.9 +/- 14.2 years were enrolled. Automated serum chemistries, complete blood cell count with differential, arterial blood gas values, and serum digoxin and theophylline levels were determined and a 12-lead electrocardiogram was obtained at the start of the trial. Following the completion of each phase of the study, a repeat physical examination was performed, and arterial blood gas values and an electrocardiogram were obtained. The trial was designed to run for two Vantin Generic Name days.

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The present study was carried out to study the effect of spironolactone, atenolol, metoprolol, ramipril and perindopril on cardiovascular complications in neonatal model of diabetes in rats, induced by administering 90 mg/kg streptozotocin (STZ), i.p. in 2-day-old rats. Our data suggest that spironolactone, metoprolol and perindopril prevent not only the STZ-induced metabolic abnormalities but also cardiovascular complications Zithromax Online Canada as evident from the reduction in cholesterol, triglyceride and decrease in cardiac hypertrophy which are the initial symptoms of congestive heart failure. Metoprolol and perindopril appears to be beneficial agents as compared to atenolol and ramipril.

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In acute myocardial infarction, beta-adrenergic blockade might depress left ventricular contractility or improve contractility by reducing ischemia. Gated equilibrium radionuclide ventriculography and Hyzaar Generic Name cuff blood pressure were employed in 10 patients to assess the left ventricular systolic pressure/volume (P/V) ratio as an index of contractility before and after intravenous metoprolol 9.3 +/- 2.5 hr after onset of infarction. In 13 normal subjects, the baseline left ventricular PV ratio was 3.5 and the left ventricular ejection fraction (LVEF) was 70%, both greater than the patients with infarction. In the patients after blockade, the systolic blood pressure decreased (p = 0.02), and the left ventricular end-systolic volume increased (p = 0.003), thus decreasing the P/V ratio from 1.7 to 1.4 (p = 0.003), while the ejection fraction (EF) was unchanged (55% versus 52%). The right ventricular ejection fraction (RVEF) decreased from 50% to 43% (p = 0.004). Thus, radionuclide ventriculography demonstrated that left ventricular contractility was reduced in patients with acute myocardial infarction and that beta-adrenergic blockade further decreased left ventricular contractility and right ventricular performance.

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Dean Health System, with medical clinics and pharmacies linked by an electronic medical record Cordarone Cost , and a shared health plan and pharmacy benefits management company.

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We have used a combination of a beta-blocker and verapamil to treat 42 consecutive patients with angina resistant to either agent alone. Patients with heart failure, heart block or uncontrolled hypertension were excluded. The mean duration of follow-up was 6.5 months. Thirty-six patients ( Zetia Generic Brand 81%) reported an improvement and the number of angina attacks was reduced from 17/week to 5/week. Side effects necessitated withdrawal of one or both drugs in 6 patients, 2 of whom developed bradyarrhythmias not solely related to drug treatment. The most common complication was mild left ventricular failure (6) treated by reducing or stopping the beta-blocker. The data suggest that the combination of verapamil and a beta-blocker may be used in a relatively unselected group of patients with difficult angina. However, as dosage adjustment and close observation may be necessary to minimise side effects, the use of this combination should be limited to hospital practice.

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NC decreased the incidence of spontaneous ventricular arrhythmias (especially VF), reduced Cx43 degradation, and improved Cx43 redistribution in myocardial infarcted zone in rats with hyper-AMI. The data of the present study indicated that NC may be a promising drug in Cleocin T Lotion Generic the future to prevent patients with AMI from lethal ventricular arrhythmias in prehospital setting.

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A double-blind crossover study was performed in 20 patients to verify the efficacy of tocainide plus metoprolol in patients with premature ventricular contractions (PVCs) class Lown greater than or equal to 2 (mean frequency greater than or equal to 30/h) judged as being "stable" by at least three basal 24-h Holter ECGs with PVC variation of less than +/- 25%. All 20 patients were submitted to a placebo period; and all were subsequently randomized to therapy with tocainide 1800 mg/day or metoprolol 200 mg/day for 15 days and then to tocainide 1800 mg + metoprolol 200 mg/day or tocainide 1200 mg + metoprolol 200 mg/day for 15 days, followed by a crossover of the two combination treatments. At steady state in every stage we controlled for plasma levels of the drugs, a 24-h Holter recording, and a 12-lead ECG. A modified Lown score was evaluated together with the Lown class. Tocainide (mean plasma level 3.3 +/- 0.7 micrograms/ml) was efficacious in 3 of 8 patients, the modified Lown score decreased from 63 +/- 32 (placebo period) to 42 +/- 27 (p less than 0.01) and Lown 4B arrhythmias were abolished in 3 of 4 patients. Metoprolol (mean plasma level 97.4 +/- 89.6 ng/ml) was efficacious in 2 of 10 patients; the modified Lown score and Lown classes did not change significantly. Administration of tocainide 1200 mg + metoprolol 200 mg obtained a positive response in 9 of 12 patients, the modified Lown score decreased significantly compared with placebo (from 53 +/- 31 to 32 +/- 30, p less than 0.01) Vytorin Generic Name and Lown 4B arrhythmias were abolished in 2 of 5 cases. Tocainide 1800 mg plus metoprolol 200 mg was scarcely tolerated owing to neurologic and gastroenteric side effects, and only three patients completed this stage with no better antiarrhythmic results compared to the lower dose. In conclusion, the combination of tocainide at 1200 mg and metoprolol 200 mg is well tolerated, efficacious in a high percentage of patients, and superior to single drug therapy in patients with stable PVCs.

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Out of the 93 invited patients, 54 (58.1%) provided informed consent. Nine saliva samples (16.7%) contained too little DNA. Call rates for CYP2D6 and CYP2C19 were 93.3% and 100%, respectively. Frequencies of genotype-predicted phenotype were 2.4%, 38.1%, 54.8%, and 4.8% for CYP2D6 poor metabolizers (PM), intermediate metabolizers (IM), extensive metabolizers (EM), and ultrarapid metabolizers (UM) respectively. For CYP2C19 genotype-predicted phenotype, frequencies were 2.2%, 15.6%, and 82.2% for PM, IM, and EM, respectively.

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This article seeks to clarify if gender-based differences occur in the pharmacokinetics of metoprolol in the elderly patients. There are a series of physiologic changes that occur in the elderly ranging from decreased hepatic blood flow to increased adiposity causing higher plasma concentrations at therapeutic doses as compared to the healthy young population.

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A double-blind controlled, randomized, parallel, multicenter 12-week study was conducted to compare the antihypertensive efficacy of lisinopril with that of metoprolol in treatment of moderate to severe hypertension. Initially, 118 patients were recruited on lisinopril and 61 on metoprolol; and for the purpose of efficacy analysis at week 8, 115 patients on lisinopril and 60 on metoprolol were included. The doses of lisinopril or metoprolol were 40-80 mg/day and 100-200 mg/day, respectively. At week 4, the pretreatment diastolic blood pressure of 111 mm Hg was decreased to 97 mm Hg (p less than 0.01) with lisinopril: metoprolol decreased the diastolic blood pressure from 110 to 99 mm Hg (p less than 0.01). Similar decreases were noted at week 8; however, the drop in blood pressure with lisinopril was not significantly different from that with metoprolol. Systolic blood pressure also demonstrated a decrease of about 18 mm Hg with lisinopril and 12 mm Hg with metoprolol (p less than 0.01). This larger decrease in systolic blood pressure with lisinopril was statistically significant at week 4 (p less than 0.05). These decreases in systolic blood pressures were maintained at week 8, again with statistical significance (p less than 0.01). Of the 118 lisinopril-treated patients, four were discontinued from lisinopril therapy because of headache, dizziness, rash, flushing, or lymphadenopathy. Four patients out of 61 (9.8%) were discontinued from metoprolol therapy because of fatigue, somnolence, asthenia, weight gain, flatulence, tremor, or bronchospasm. In conclusion, lisinopril 40-80 mg once daily is as effective as metoprolol 100-200 mg once daily in reducing diastolic blood pressure in patients with moderate to severe hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

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In a porcine model of HF, SCS induces significant remodelling of cardiac sympathetic innervation over the peri-infarct and infarct regions and is associated with improved LV function and reduced myocardial norepinephrine spillover.