atrial-natriuretic-factor and Thrombosis

The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study is the first, and, so far, the only endpoint trial in patients with hypertension and left ventricular hypertrophy (LVH) to show a divergent therapeutic outcome of one treatment modality over another with equivalent blood pressure control. The purpose of this article is to review post hoc sub-analyses of LIFE study data and other clinical studies that offer some insight into possible treatment-related differences contributing to the superior stroke outcome of losartan versus atenolol beyond blood pressure reduction.. Relevant randomized clinical trials and review articles were identified through a MEDLINE search of English-language articles published between 1990 and 2006 using the search terms losartan, atenolol, LIFE, hypertension, and LVH. Articles describing major clinical studies, new data, or mechanisms pertinent to the LIFE study were selected for review.. Differences in blood pressure or in the distribution of add-on medications were not evident between study groups in the LIFE study. Thus, the observed outcomes benefits favoring losartan may involve other possible mechanisms, including differential effects of losartan and atenolol on LVH regression, left atrial diameter, atrial fibrillation, brain natriuretic peptide, vascular structure, thrombus formation/platelet aggregation, serum uric acid, albuminuria, new-onset diabetes, and lipid metabolism. Alternative explanations for the LIFE study findings have also been put forward, including the choice of atenolol as an appropriate active comparator and differential effects between treatment groups on central pulse pressure. Additional clinical trials are needed to determine if the beneficial effects of losartan seen in LIFE are shared by other inhibitors of the renin-angiotensin system.. Sub-analyses of the LIFE study data suggest that losartan's stroke benefit may arise from a mosaic of mechanisms rather than a single action. Further studies are expected to continue to delineate the mechanisms of differential responses to treatments in LIFE.

Topics: Adrenergic beta-Antagonists; Angiotensin II Type 1 Receptor Blockers; Antihypertensive Agents; Atenolol; Atrial Fibrillation; Atrial Natriuretic Factor; Biomarkers; Blood Pressure; Cardiovascular Agents; Cohort Studies; Drug Utilization; Endothelium, Vascular; Follow-Up Studies; Heart Atria; Humans; Hypertension; Hypertrophy, Left Ventricular; Losartan; Models, Biological; Myocardial Infarction; Natriuretic Peptide, Brain; Peptide Fragments; Platelet Aggregation; Platelet Aggregation Inhibitors; Protein Precursors; Randomized Controlled Trials as Topic; Research Design; Risk; Risk Factors; Stroke; Thrombosis; Treatment Outcome

This update reviews the remarkable progression in several cardiovascular gene transfer domains. The first chemical gene therapy protocols to stimulate angiogenesis in ischemic myocardium are discussed and both the great expectations as well as remaining hurdle are highlighted. In experimental models of restenosis and heart failure gene therapy shows promising results. Important question regarding vector-related limitations and suboptimal in vivo delivery systems will require expeditious attention for gene therapy to become a more widely applicable option in cardiovascular diseases.

Topics: Animals; Arteriosclerosis; Atrial Natriuretic Factor; Cardiovascular Diseases; Coronary Disease; Endothelial Growth Factors; Gene Transfer Techniques; Genetic Therapy; Genetic Vectors; Heart Failure; Humans; Hypertension; Lymphokines; Mice; Neovascularization, Physiologic; Rabbits; Superoxide Dismutase; Thrombosis; Tissue Plasminogen Activator; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factors

Several studies have reported that the use of a distal protection device decreases the incidence of slow-flow and/or no-reflow in patients with myocardial infarctions. In the present study, we investigated the influence of a RESCUE/Thrombuster system and a PercuSurge GuardWire catheter on coronary microcirculation disorders in patients with acute myocardial infarction using the natriuretic polypeptide (ANP), the brain natriuretic peptide (BNP), and (99m)Tc-tetrofosmin myocardial scintigraphy (TF). The group consisted of a 77 patients with initial inferior myocardial infarction who had undergone emergency coronary angioplasty. The patients were randomly divided into: Group D (n=28), in which a direct stent alone was inserted, Group R/T (n=25), in which a stent was inserted after RESCUE system or a Thrombuster system was performed, and Group P (n=24), in which a stent was inserted after thrombus suction using a PercuSurge GuardWire catheter. Patients with coronary slow-flow/no-reflow were 3, 2 and 0 cases in Group D, Group R / T and Group P, respectively. In the present study, patients with good-reflow were enrolled in order to investigate the coronary microcirculation disorder in patients with visually similar coronary blood flow obtained in coronary angiography after percutaneous coronary reperfusion therapy. TF myocardial scintigraphy was performed 10+/-3 days after admission. Bull's eye images were divided into 8 sections, and each section was evaluated in 4 grades. The grade of each segment was regarded as the defect score. The results were compared with the database prepared based on bull's eye maps from 50 healthy adults in our hospital, and count areas of -2 x SD (standard deviation) or less were calculated as the extent score (%), reflecting the area in which myocardial blood flow was decreased. The extent and severity scores in Groups P and R/T were significantly lower than those in Group D. Coronary angiography at the chronic stage (6 months after surgery) showed the patency of the responsible vascular lesion in all patients. However, the ANP, BNP, cardiac index, and pulmonary capillary wedge pressure (PCWP) were significantly improved in Groups R/T and P, compared to Group D (p<0.01). These results suggest that the use of a RESCUE/Thrombuster system and a PercuSurge GuardWire catheter system in patients with acute inferior wall infarction improves coronary microcirculation disorders and acute- to chronic-phase cardiac function.

Topics: Aged; Atrial Natriuretic Factor; Coronary Circulation; Humans; Male; Middle Aged; Myocardial Infarction; Natriuretic Peptide, Brain; Radionuclide Imaging; Stents; Suction; Thrombectomy; Thrombosis

The clinical relevance of examining human atrial natriuretic peptide (HANP) or left atrial appendage (LAA) wall-motion velocity during sinus rhythm in paroxysmal atrial fibrillation (AF) patients has not been clearly elucidated.. The subjects were 38 patients with paroxysmal AF who underwent transesophageal and transthoracic echocardiography during sinus rhythm. The presence of spontaneous echocontrast (SEC) was examined with transesophageal echocardiography and LAA wall-motion velocity (LAAWV) was measured with transthoracic tissue Doppler echocardiography. Plasma HANP was measured within 3 hours after echocardiography.. Human atrial natriuretic peptide ranged from 12 to 106 pg/mL with an average of 43 ± 24 pg/mL and had a significant correlation with LAAWV (r = -0.57) or LAA flow velocity (r = -0.41). HANP was significantly higher in patients with SEC than in patients without SEC (64 ± 29 vs. 34 ± 15 pg/mL, P = 0.008) and LAAWV was significantly lower in patients with SEC than in patients without SEC (13 ± 5 vs. 20 ± 5 cm/sec, P = 0.002). HANP >44 pg/mL had a sensitivity of 73% and specificity of 89% for diagnosing SEC. SEC was more frequently observed (73%) in patients with HANP >44 pg/mL and/or LAAWV <10 cm/sec as compared with patients (11%) with normal HANP and LAA wall-motion velocity (P < 0.0001).. Higher plasma HANP and lower LAA wall-motion velocity may be noninvasive surrogate markers for assessing left atrial thrombogenesis during sinus rhythm in paroxysmal AF patients.

Topics: Aged; Atrial Appendage; Atrial Fibrillation; Atrial Natriuretic Factor; Biomarkers; Echocardiography; Female; Humans; Male; Prognosis; Reproducibility of Results; Retrospective Studies; Sensitivity and Specificity; Thrombosis

Cardiac hypertrophy and function were studied 6 wk after constriction of the thoracic aorta (TAC) in transgenic (TG) mice expressing constitutively active mutant alpha(1B)-adrenergic receptors (ARs) in the heart. Hearts from sham-operated TG animals and nontransgenic littermates (WT) were similar in size, but hearts from TAC/TG mice were larger than those from TAC/WT mice, and atrial natriuretic peptide mRNA expression was also higher. Lung weight was markedly increased in TAC/TG animals, and the incidence of left atrial thrombus formation was significantly higher. Ventricular contractility in anesthetized animals, although it was increased in TAC/WT hearts, was unchanged in TAC/TG hearts, implying cardiac decompensation and progression to failure in TG mice. There was no increase in alpha(1A)-AR mRNA expression in TAC/WT hearts, and expression was significantly reduced in TAC/TG hearts. These findings show that cardiac expression of constitutively actively mutant alpha(1B)-ARs is detrimental in terms of hypertrophy and cardiac function after pressure overload and that increased alpha(1A)-AR mRNA expression is not a feature of the hypertrophic response in this murine model.

Topics: Adrenergic alpha-1 Receptor Antagonists; Adrenergic alpha-Antagonists; Animals; Aorta, Thoracic; Atrial Natriuretic Factor; Binding, Competitive; Blood Pressure; Cardiac Myosins; Cardiomegaly; Constriction, Pathologic; Down-Regulation; Heart; Lung; Mice; Mice, Inbred Strains; Mice, Transgenic; Myocardium; Myosin Light Chains; Organ Size; Pressure; Promoter Regions, Genetic; Radioligand Assay; Receptors, Adrenergic, alpha-1; RNA, Messenger; Thrombosis

Topics: Animals; Atrial Appendage; Atrial Natriuretic Factor; Disease Models, Animal; Dogs; Goats; Guinea Pigs; Heart Diseases; Hemodynamics; Humans; Hypertrophy; Sheep; Stroke; Thirst; Thrombosis