Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study was designed to assess the antihypertensive effect of combined angiotensin-converting enzyme (ACE) inhibition and angiotensin II type 1 receptor (AT1) antagonism in patients with essential hypertension. Twenty patients with uncontrolled ambulatory diastolic blood pressure (BP) after 6 weeks of ACE inhibitor monotherapy (benazepril, 20 mg, o.d.) were randomized to receive double-blind valsartan, 80 mg, o.d. (AT1 antagonist) or matching placebo for 5 weeks while continuing to receive background benazepril. Then patients crossed over to the alternative regimen for a second 5-week period. The 24-h ambulatory BP was monitored on the final day of the benazepril monotherapy period and on the final day of each double-blind treatment period. Valsartan added to benazepril produced a significant antihypertensive effect with a benefit over placebo of 6.5 +/- 12.6/4.5 +/- 8.0 mm Hg (systolic/diastolic) for average awake ambulatory BP (p < 0.05), 7.1 +/- 9.4/5.6 +/- 6.5 mm Hg for asleep BP (p < 0.01), and 6.8 +/- 9.7/4.9 +/- 6.8 mm Hg for average 24-h ambulatory BP (p < 0.01). Pulse rate was unaffected. Plasma active renin was higher on the benazepril-valsartan combination compared with benazepril-placebo (p < 0.05). There was no change in routine biochemical variables when valsartan was added to benazepril. Six patients reported mild dizziness or fatigue (three also with placebo). These data suggest that in hypertensive patients uncontrolled with an ACE inhibitor, the addition of an AT1 antagonist provides a powerful and safe antihypertensive drug combination.
J Cardiovasc Pharmacol 2000 Jun
PMID:Additive hypotensive effect of angiotensin-converting enzyme inhibition and angiotensin-receptor antagonism in essential hypertension. 1083 30

The objective of this study was to assess the electrophysiological properties of intravenous bisoprolol in patients with and without coronary artery disease (CAD) by programmed stimulation. Sixteen inpatients subjected to an electrophysiological investigation because of dizziness or palpitations were given 10 mg of intravenous bisoprolol after basal measurement and were checked again 15 and 45 min after infusion. Eight patients with CAD (seven males and one female; mean age of 60+/-4 years) and eight patients without CAD (five males and three females; mean age of 59+/-4 years) were investigated after washout of prior antiarrhythmic drugs. For coronary patients, the CAD was documented by a history of myocardial infarction or by a confirmatory coronary arteriography. Main outcome measures were parameters of invasive electrophysiological exploration, with measurement of conduction intervals at rest and during pacing and of refractory periods by means of extrastimulus technique. No significant difference was noted at baseline between the two groups except for CSNRT. After infusion of 10 mg of bisoprolol, with the exception of CSNRT (increased in the group without CAD), no significant differences were noted on comparison between coronary and noncoronary patients. Bisoprolol significantly increased the sinus cycle length, SACT, and FRP of the atria. Regarding atrioventricular nodal conduction, bisoprolol significantly increased the AH 100, ERP, and FRP and significantly decreased the Wenckebach point. In the right ventricle, bisoprolol moderately, but significantly, decreased the corrected QT and induced a small, temporary, significant increase in ERP. Bisoprolol appears to be a very potent beta-blocker that is well tolerated at an intravenous dose of 10 mg. Its depressant effects concern mainly the atrial function and the nodal conduction, without significant differences between the two groups of patients. The decrease in QTc may be a favorable aspect regarding its electrophysiologic tolerance especially in the acute phase of myocardial infarction.
J Cardiovasc Pharmacol 1990
PMID:Study of the electrophysiological properties of intravenous bisoprolol in patients with and without coronary artery disease by programmed stimulation. 1152 22

The safety and efficacy of endoluminal stenting in treating atherosclerotic vertebral artery disease was evaluated in 38 vessels in 32 patients. Indications for revascularization included diplopia (n = 4), blurred vision (n = 4), dizziness (n = 23), transient ischemic attacks (n = 4), drop attack (n = 1), gait disturbance (n = 1), headache (n = 2), and asymptomatic critical stenosis (n = 1). Success (< 20% residual diameter stenosis, without stroke or death) was achieved in all 32 patients (100%). One patient experienced a transient ischemic attack (TIA) 1 hr after the procedure. At follow-up (mean, 10.6 months), all patients (100%) were alive and 31/32 (97%) were asymptomatic. One patient (3%) had in-stent restenosis at 3.5 months and underwent successful balloon angioplasty. Endoluminal stenting of vertebral artery lesions is safe, effective, and durable as evidenced by the low recurrence rate. Primary stent placement is an attractive option for atherosclerotic vertebral artery stenotic lesions. Cathet Cardiovasc Intervent 2001;54:1-5.
Catheter Cardiovasc Interv 2001 Sep
PMID:Vertebral artery stenting. 1155 40

Dissection of the cervical segment of the internal carotid artery may occur spontaneously or after trauma. We report the management of a 53-year-old right-handed man with progressive dizziness and neck pain 6 weeks after a motor vehicle collision. The clinical and neurologic examinations were normal. The CT scan led to the diagnosis of a pseudoaneurysm of the right internal carotid artery near the skull base. We successfully treated this post-traumatic lesion with a covered stent. The patient underwent the endovascular procedure under general anesthesia and transcranial Doppler monitoring. No neurologic event was observed. Obliteration of the pseudoaneurysm with preservation of the carotid artery was achieved. The patient was discharged from the hospital 72 hr later with no complications. Clinical and imaging follow-up at 6 months was unremarkable.
Cardiovasc Intervent Radiol
PMID:Pseudoaneurysm of the internal carotid artery: treatment with a covered stent. 1177 22

Cilostazol (Pletal), a quinolinone derivative, has been approved in the U.S. for the treatment of symptoms of intermittent claudication (IC) since 1999 and for related indications since 1988 in Japan and other Asian countries. The vasodilatory and antiplatelet actions of cilostazol are due mainly to the inhibition of phosphodiesterase 3 (PDE3) and subsequent elevation of intracellular cAMP levels. Recent preclinical studies have demonstrated that cilostazol also possesses the ability to inhibit adenosine uptake, a property that may distinguish it from other PDE3 inhibitors, such as milrinone. Elevation of interstitial and circulating adenosine levels by cilostazol has been found to potentiate the cAMP-elevating effect of PDE3 inhibition in platelets and smooth muscle, thereby augmenting antiplatelet and vasodilatory effects of the drug. In contrast, elevation of interstitial adenosine by cilostazol in the heart has been shown to reduce increases in cAMP caused by the PDE3-inhibitory action of cilostazol, thus attenuating the cardiotonic effects. Cilostazol has also been reported to inhibit smooth muscle cell proliferation in vitro and has been demonstrated in a clinical study to favorably alter plasma lipids: to decrease triglyceride and to increase HDL-cholesterol levels. One, or a combination of several of these effects may contribute to the clinical benefits and safety of this drug in IC and other disease conditions secondary to atherosclerosis. In eight double-blind randomized placebo-controlled trials, cilostazol significantly increased maximal walking distance, or absolute claudication distance on a treadmill. In addition, cilostazol improved quality of life indices as assessed by patient questionnaire. One large randomized, double-blinded, placebo-controlled, multicenter competitor trial demonstrated the superiority of cilostazol over pentoxifylline, the only other drug approved for IC. Cilostazol has been generally well-tolerated, with the most common adverse events being headache, diarrhea, abnormal stools and dizziness. Studies involving off-label use of cilostazol for prevention of coronary thrombosis/restenosis and stroke recurrence have also recently been reported.
Cardiovasc Drug Rev 2001
PMID:Cilostazol (pletal): a dual inhibitor of cyclic nucleotide phosphodiesterase type 3 and adenosine uptake. 1183 Jul 53

The purpose of this paper is to review the role of doxazosin, a long-acting alpha(1)-blocker, as a component of combination therapy for patients with stage 1 and stage 2 hypertension and for patients with concomitant hypertension and hyperlipidemia or glucose intolerance. Recent studies that evaluated doxazosin as combination therapy in the treatment of patients with inadequately controlled hypertension and patients with concomitant hypertension and other disorders were reviewed. Data extraction was based on the tolerability and efficacy data of doxazosin in patients with hypertension. Compared with placebo, doxazosin combination therapy leads to significant improvements in sitting and standing blood pressure. Doxazosin is well tolerated, with only minor adverse effects (e.g., headache, dizziness) as the most commonly reported treatment-related complications. The studies described demonstrate that doxazosin is effective as combination therapy for patients with stage 1 and stage 2 hypertension. The positive effects of doxazosin on serum lipids make combination therapy with doxazosin an attractive treatment option for patients who have concomitant hyperlipidemia or glucose intolerance.
J Cardiovasc Pharmacol 2003 Jun
PMID:Doxazosin as combination therapy for patients with stage 1 and stage 2 hypertension. 1277 63

Closure of patent foramen ovale (PFO) has been proposed as an alternative to anticoagulation in patients with presumed paradoxical emboli. We report the immediate and mid-term results of the phase 1 U.S. Multicenter Clinical Trial of patients who underwent transcatheter PFO closure for paradoxical embolism using the new Amplatzer PFO device. Fifty patients (28 male/22 female) underwent catheter closure of their PFOs at a mean age of 41 +/- 11 years. Thirty-six patients had ischemic stroke, 10 had transient ischemic attack, and 4 had peripheral embolism. Seventeen patients had atrial septal aneurysm. The implantation procedure was successful in 49/49 patients; one patient did not have a PFO. Complete closure was seen immediately after the procedure in 26/49 patients; 17 had minimal residual shunt, 4 had moderate and 2 had large residual shunts. The median fluoroscopy time was 10.5 min (2.8-43 min). There were no complications related to the device. One patient developed an arteriovenous fistula at the catheter site requiring surgical repair. At a mean follow-up interval of 16.5 +/- 7.2 months, there were no deaths or recurrent neurological or peripheral embolic events. Eight patients reported an episode of dizziness or palpitations (four of them within 18 days of the procedure). No episodes of atrial dysrhythmias were noted. Contrast bubble study at last follow-up documented complete closure in 45/48 patients; one patient had minimal, one had moderate residual shunt, and one had a large shunt. One patient was lost to follow-up. We conclude that catheter closure of PFO associated with stroke/transient ischemic attack or peripheral embolism using the new Amplatzer PFO device is a safe and effective method in preventing recurrence of such episodes. Randomized clinical trials comparing device closure versus continued medical therapy are underway.
Catheter Cardiovasc Interv 2003 Dec
PMID:Transcatheter closure of patent foramen ovale associated with paradoxical embolism using the amplatzer PFO occluder: initial and intermediate-term results of the U.S. multicenter clinical trial. 1462 34

Bosentan is a nonpeptide, specific, competitive, dual antagonist at both endothelin receptor subtypes (ET(A) and ET(B)). Orally administered bosentan effectively prevents endothelin 1-induced vasoconstriction in pulmonary vessels in patients with pulmonary arterial hypertension. Improvement in exercise capacity from baseline was significantly greater with bosentan than with placebo in two phase III trials in patients with WHO functional class III or IV pulmonary arterial hypertension (primary or associated with connective tissue disease) despite treatment with vasodilators, diuretics, anticoagulants, cardiac glycosides, or supplemental oxygen. The beneficial effects of bosentan on exercise capacity were maintained for at least 20 weeks. Compared with placebo, bosentan led to a significantly greater improvement from pretreatment values in secondary efficacy endpoints such as the Borg dyspnea index, WHO functional class, and cardiopulmonary hemodynamic parameters (cardiac index, pulmonary vascular resistance, pulmonary artery pressure, pulmonary capillary wedge pressure, mean right atrial pressure). Bosentan significantly reduced the incidence, and delayed the onset, of clinical worsening of pulmonary arterial hypertension compared with placebo. In published clinical trials, adverse events that occurred with similar or greater frequency with bosentan 125 mg twice daily than with placebo included headache, syncope, flushing and abnormal hepatic function. Those that occurred less frequently with bosentan 125 mg twice daily than with placebo included dizziness, worsening of symptoms of pulmonary arterial hypertension, cough and dyspnea.
Am J Cardiovasc Drugs 2002
PMID:Bosentan. 1472 63

Valsartan, an orally active nonpeptide angiotensin II (AII) receptor antagonist with selectivity for the AII type I (AT(1)) receptor subtype, has recently been approved by the US Food and Drug Administration for the treatment of patients with heart failure (New York Health Association class II-IV) who are intolerant of ACE-inhibitor therapy. Results from the Valsartan Heart Failure Trial (Val-HeFT) showed that in patients with chronic heart failure (CHF) [n = 5010], valsartan 160 mg twice daily, when used in combination with conventional therapy for heart failure, reduced the risk of the combined endpoint of mortality and morbidity by 13.2% compared with placebo. However, there was no significant difference in overall mortality between the valsartan and placebo groups. Morbidity was defined as cardiac arrest with resuscitation, hospitalization for heart failure, or administration of intravenous inotropic or vasodilator drugs for > or =4 hours without hospitalization. Among patients not receiving an ACE inhibitor, irrespective of concomitant beta-blocker use, valsartan reduced the risk of mortality and the combined endpoint by 33.1% and 44% compared with placebo; total hospitalizations for heart failure were also significantly lower in the valsartan group (27.6 vs 64.6%). In the subgroup of patients who were taking an ACE inhibitor and a beta-blocker at baseline (n = 1610), mortality was significantly higher in the valsartan group than in the placebo group. The most common adverse events in the valsartan and placebo groups which led to discontinuation of treatment were dizziness, renal impairment (both of which occurred in significantly more valsartan recipients) and hypotension.
Am J Cardiovasc Drugs 2002
PMID:Valsartan: in chronic heart failure. 1472 72

Controlled clinical trials performed in more than 13 000 patients have, to date, consistently shown the beneficial effects of long term beta-adrenoceptor antagonist (beta-blocker) therapy in patients with chronic heart failure. It is not clear whether this represents a class effect or whether it is specific only to some agents. Beneficial effects on the prognosis of patients with mild to moderate heart failure have been shown with metoprolol, bisoprolol, and carvedilol. These beta-blockers, however, differ in their pharmacologic characteristics. Metoprolol and bisoprolol are selective for beta(1)-adrenergic receptors and are devoid of ancillary properties. Carvedilol, at a dosage of 50 mg/day, blocks all beta(1)-, beta(2)-, and alpha(1)-adrenergic receptors, and it has associated antiproliferative and antioxidant activities. These differences cause a varied acute hemodynamic response, with a reduction in cardiac output and a tendency toward a rise in pulmonary wedge pressure with selective agents and no change in cardiac output and a slight decrease in pulmonary pressures with carvedilol. Accordingly, when the therapy is started, the most frequent adverse effects are worsening heart failure with metoprolol and bisoprolol, and hypotension and dizziness with carvedilol. It remains controversial whether these differences also influence the long term effects of therapy. Carvedilol may provide a more comprehensive blockade of the cardiac adrenergic drive than selective beta-blockers because it does not upregulate beta(1)-adrenergic receptors, blocks all adrenergic receptors and decreases cardiac norepinephrine release. These properties may lead to a larger increase in left ventricular function and a lack of improvement in maximal exercise capacity with carvedilol, compared with selective beta-blockers. It is, however, unclear whether these differences also influence patient outcome. The long term effects of different beta-blockers on prognosis are currently being compared in the Carvedilol or Metoprolol European Trial (COMET) in which more than 3000 patients with chronic heart failure have been randomized in a 1 : 1 ratio to receive metoprolol or carvedilol.
Am J Cardiovasc Drugs 2001
PMID:Beta-blockade in heart failure: selective versus nonselective agents. 1472 47


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>