Biomedical subjects

T L Lenz

Publications and source records attributed to T L Lenz.

5 recordsLinked to original sources

PubMed2001

Comparison of 24-hour blood pressure profiles in patients with hypertension who were switched from amlodipine to nisoldipine.

STUDY OBJECTIVE: To compare 24-hour blood pressure control and adverse effects in patients with essential hypertension who were switched from amlodipine to nisoldipine. DESIGN: Open-label, one-way crossover study. SETTING: Cardiac clinic and patients' homes. PATIENTS: Twenty-five patients with stage I or II essential hypertension stabilized with amlodipine for at least 3 months, of whom 21 patients completed the study. INTERVENTION: All patients underwent 24-hour ambulatory blood pressure monitoring while receiving amlodipine 5 or 10 mg/day. Patients then were switched to nisoldipine 10 mg/day (> or = 65 yrs old) or 20 mg/day (< 65 yrs old) and returned to the clinic at 2-week intervals to assess cuff blood pressure, heart rate, adverse effects, and compliance. No adverse effects were experienced in 15 of the 25 patients. Lower extremity edema was the most commonly reported adverse effect (four patients). Two patients discontinued treatment because of pulmonary edema in one and chest pain in the other. Two patients were lost to follow-up. After a mean of 10.6 weeks, repeat 24-hour ambulatory monitoring was performed to evaluate blood pressure control with nisoldipine. Systolic and diastolic ambulatory results for daytime, nighttime, and total 24 hours were calculated. For amlodipine versus nisoldipine, no significant differences existed in any of the blood pressure parameters (p>0.05) in the 21 patients who completed the study, except for 24-hour diastolic pressure (p<0.05); however, this latter difference was only 2 mm Hg (nisoldipine 77 mm Hg, amlodipine 75 mm Hg). CONCLUSION: Both amlodipine and nisoldipine have similar 24-hour ambulatory blood pressure profiles. The frequency of lower extremity edema was no different after the switch to nisoldipine than when the patients were taking amlodipine.

Adult↗

PubMed2001

Therapeutic change of HMG-CoA reductase inhibitors in patients with coronary artery disease.

STUDY OBJECTIVE: To evaluate short-term outcomes when atorvastatin was substituted for pravastatin or simvastatin in patients with coronary artery disease. DESIGN: Open-label, fixed-dosage, one-way crossover from pravastatin and simvastatin to atorvastatin. SETTING: University-affiliated hospital and outpatient clinics. PATIENTS: Eighty patients with coronary artery disease with a minimum baseline low-density lipoprotein (LDL) above 130 mg/dl: 20 were treated with pravastatin 20 mg/day, 20 with pravastatin 40 mg/day, 20 with simvastatin 20 mg/day, and 20 with simvastatin 40 mg/day for a minimum of 6 months, with a prescription refill rate of 80% or greater. Intervention. Before crossover, patients had a fasting lipid profile determined and were questioned about side effects of pravastatin and simvastatin. All patients were switched to atorvastatin 10 mg/day. After 12 weeks of atorvastatin therapy, a repeat fasting lipid profile was obtained and patients were questioned about side effects with the drug. MEASUREMENTS AND MAIN RESULTS: Baseline demographic and clinical characteristics of the treatment groups were not significantly different with the exception of a lower baseline LDL in patients receiving pravastatin 20 mg/day. Baseline LDL values were as follows: pravastatin 20 mg/day, 158+/-26 mg/dl; pravastatin 40 mg/day, 176+/-22 mg/dl; simvastatin 20 mg/day, 177+/-27 mg/dl; and simvastatin 40 mg/day, 177+/-27 mg/dl. Reductions in LDL after treatment with pravastatin or simvastatin were as follows: pravastatin 20 mg/day, 22%; pravastatin 40 mg/day, 32%; simvastatin 20 mg/day, 33%; and simvastatin 40 mg/day, 38%. Patients achieving LDL goal with initial therapy were as follows: pravastatin 20 mg/day, 5%; pravastatin 40 mg/day, 5%; simvastatin 20 mg/day, 20%; and simvastatin 40 mg/day, 30%. After the switch to atorvastatin 10 mg/day, reductions in LDL were as follows: pravastatin 20 mg/day, 39% (p<0.001); pravastatin 40 mg/day, 38% (p<0.01); simvastatin 20 mg/day, 39% (p=0.04); and simvastatin 40 mg/day, 38% (p=0.83). Patients achieving LDL goals with atorvastatin 10 mg/day were as follows: pravastatin 20 mg/day, 60%; pravastatin 40 mg/day, 30%; simvastatin 20 mg/day, 25%; and simvastatin 40 mg/day, 30%. The frequency of side effects was similar for all three statins. Based on annual average wholesale price, atorvastatin 10 mg/day was more cost-effective than all pravastatin and simvastatin regimens. CONCLUSIONS: Therapeutic interchange from pravastatin 20 and 40 mg/day and simvastatin 20 mg/day to atorvastatin 10 mg/day was associated with both cost savings and significant reductions in LDL. The change from simvastatin 40 mg/day to atorvastatin 10 mg/day was associated with cost savings and an equivalent reduction in LDL.

Atorvastatin↗

PubMed2000

Aggrenox: a fixed-dose combination of aspirin and dipyridamole.

OBJECTIVE: To describe the pharmacology, pharmacokinetics, efficacy, and safety of a fixed-dose combination of aspirin and extended-release (ER) dipyridamole indicated for the secondary prevention of stroke. DATA SOURCES: Published articles and abstracts were identified from a MEDLINE search (1966-December 1999) using the search terms dipyridamole, aspirin, antiplatelet, antiaggregation, and stroke prevention. Pertinent articles written in English were considered for review. Additional articles were identified from the references of retrieved literature. STUDY SELECTION AND DATA EXTRACTION: Studies including a combination of aspirin/dipyridamole in human subjects were evaluated. Emphasis was placed on randomized, controlled trials. DATA SYNTHESIS: Aspirin is a platelet inhibitor that works by inhibiting platelet cyclooxygenase, which reduces the production of thromboxane A2. Dipyridamole is a platelet inhibitor that is thought to work in part by inhibiting platelet cyclic-3',5'-adenosine monophosphate and cyclic-3',5'-guanosine monophosphate phosphodiesterase. The active metabolite of aspirin, salicylic acid, is highly bound to plasma protein and has a plasma half-life of two to three hours. Dipyridamole is also highly bound to plasma proteins, and the ER formulation has a plasma half-life of 13 hours. The first European Stroke Prevention Study (ESPS-1) found the combination of aspirin/dipyridamole to be superior to placebo in the prevention of stroke and transient ischemic attack (TIA). The ESPS-1, however, did not include an aspirin-only treatment arm. Therefore, it was unclear whether the combination of aspirin/dipyridamole was superior to aspirin alone. As a result, a second trial was conducted that included treatment arms of aspirin alone, ER dipyridamole alone, combination therapy, and placebo. The combination of aspirin 25 mg plus ER dipyridamole 200 mg twice daily was shown in the ESPS-2 to be significantly better than either agent given individually in preventing stroke and TIAs (p < 0.001). CONCLUSIONS: The American College of Chest Physicians (ACCP) recommends aspirin 50-325 mg/d to be the initial antiplatelet of choice for the prevention of atherothrombotic cerebral ischemic events. However, with the favorable results of the ESPS-2, it may be appropriate to substitute aspirin/ER dipyridamole for aspirin alone as the drug of choice. This combination appears to have a favorable adverse effect profile. The relative effectiveness of aspirin/ER dipyridamole compared with clopidogrel and ticlopidine has yet to be determined. If alternative antiplatelet therapy is needed, the ACCP recommends clopidogrel rather than ticlopidine because of its lower incidence of adverse effects. The ACCP further states that the combination of aspirin plus dipyridamole may be more effective than clopidogrel; these agents have a similarly favorable adverse effect profile.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2000

Dofetilide: A new antiarrhythmic agent approved for conversion and/or maintenance of atrial fibrillation/atrial flutter.

Dofetilide is a new antiarrhythmic agent recently approved for the conversion of and maintenance of sinus rhythm in patients with atrial fibrillation (AF) and atrial flutter (AFl). Dofetilide is a selective class III antiarrhythmic drug which works by selectively blocking the rapid component of the delayed rectifier outward potassium current (I(kr)). Dofetilide has been shown to prolong the effective refractory period which is accompanied by a dose-dependent prolongation of the QT and QTc intervals, with parallel increases in ventricular refractoriness. Approximately 80% of dofetilide is excreted in the urine which requires dose adjustments in renal insufficiency. The elimination half-life is approximately 10 h in patients with normal renal function. The therapeutic blood level range of dofetilide is presently unknown and monitoring of dofetilide blood levels is not available at this time. Clinical trials have shown dofetilide to be superior to flecainide in converting AFl patients to normal sinus rhythm (NSR) (70% vs. 9%; p<0.01). It also was more effective than sotalol in converting AF and AFl patients to NSR (29% vs. 6%; p<0.05) and maintaining these patients in NSR for up to 1 year (p<0.05). Most patients convert to NSR within 24-36 h. Torsade de pointes is the most serious side effect occurring in 0.3-10.5% of patients and is dose related. Other common side effects include headache, chest pain and dizziness. To minimize the risk of induced arrhythmia, patients initiated or reinitiated on dofetilide should be hospitalized for a minimum of 3 days where continuous electrocardiographic monitoring, evaluation of renal function and serum electrolytes and cardiac resuscitation can be provided.

Journal Article↗

PubMed2000

Dofetilide, a new class III antiarrhythmic agent.

Dofetilide is a new antiarrhythmic agent recently approved for conversion and maintenance of sinus rhythm in patients with atrial fibrillation (AF) and atrial flutter (AFl). It is a class III antiarrhythmic that works by selectively blocking the rapid component of the delayed rectifier outward potassium current. Dofetilide prolongs the effective refractory period in accessory pathways, both anterograde and retrograde. This can be seen on the electrocardiogram through a dose-dependent prolongation of the QT and QTc intervals, with parallel increases in ventricular refractoriness. Approximately 80% of drug is excreted in urine, so dosing must be based on creatinine clearance. The elimination half-life is approximately 10 hours. In clinical trials dofetilide was superior to flecainide in converting patients with AFl to normal sinus rhythm (NSR; 70% vs 9%, p<0.01). It also was more effective than sotalol in converting patients with both AF and AFl to NSR (29% vs 6%, p<0.05) and maintaining them in NSR for up to 1 year. Most patients converted within 24-36 hours. Dofetilide has a favorable risk:benefit profile. Torsades de pointes is the most serious side effect; it occurs in 0.3-10.5% of patients and is dose related. To minimize the risk of induced arrhythmia, patients who start or restart the drug should be hospitalized a minimum of 3 days for creatinine clearance measurements, continuous electrocardiographic monitoring, and cardiac resuscitation, if necessary.

Animals↗