Closed relation between carotid and ascending aortic atherosclerosis in cardiac patients.

BACKGROUND: Carotid atherosclerosis and aortic atherosclerosis are both associated with coronary artery disease and cerebral thromboembolism. However, the relationship between asymptomatic carotid and aortic atherosclerosis is not well known. METHODS AND RESULTS: Sixty-two consecutive cardiac patients (mean age 57 years) without a history of atherosclerotic cardiovascular disease who were referred for transesophageal echocardiography were included. By means of a high-resolution ultrasound technique, normal carotid arteries were found in 12 patients (19.4%), whereas 15 patients (24. 2%) had increased intima-media thickness, and the remaining 35 patients (56.5%) had atherosclerotic plaques (intima-media thickness >/=1.3 mm). Transesophageal echocardiography characterized ascending aortic intimal morphology as normal in 1 patient (1.6%), as thickening in 22 patients (35.5%), and as atherosclerotic plaques in 39 patients (62.9%). Patients with both carotid and aortic plaques were older compared with patients without plaques; also, a higher percentage of patients with carotid and aortic plaques suffered from hypertension and diabetes mellitus compared with patients without plaques (P:<0.001). The incidence of carotid plaques was 74.3% (29 of 39 patients) in the subgroup with aortic plaques; there was a stepwise increase in the percentage of patients with carotid plaques among the patients with increasing grades of aortic atherosclerosis. Furthermore, the incidence of ascending aortic plaques was 82.8% (29 of 35 patients) in the subgroup with carotid plaques. Regression analysis revealed that age and carotid plaques were independently related to the presence of aortic plaques. In the entire study population, the presence of carotid plaques had a high positive predictive value (83%), an acceptable sensitivity (75%) and specificity (74%), and a relatively low negative predictive value (63%) for the presence of aortic plaques. CONCLUSIONS: In cardiac patients without clinical evidence of atherosclerotic cardiovascular disease, a high prevalence of combined aortic and carotid plaques were detected. The presence of carotid plaque reflects the presence of aortic plaque, whereas the absence of carotid plaque may not reflect the absence of aortic plaque.

Dyslipidemic effects of cigarette smoking on beta-blocker-induced serum lipid changes in systemic hypertension.

To assess the effects of beta blockers on lipids and apolipoproteins in cigarette smokers and nonsmokers, 330 patients with systemic hypertension received 1 month of placebo and 6 months of beta-blocker monotherapy. Serum total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and apolipoproteins A1 and B were measured. Total cholesterol increased with propranolol (smokers vs nonsmokers, 8 vs 2%); increased for smokers and decreased for nonsmokers with atenolol (8 vs -3%), metoprolol (6 vs -1%) and pindolol (7 vs -6%); and decreased for both groups with celiprolol (-3 vs -10%). HDL cholesterol decreased with propranolol (smokers vs nonsmokers, -8 vs -18%), atenolol (-7 vs -2%) and metoprolol (-12 vs -1%); increased for smokers and decreased for nonsmokers with pindolol (11 vs -2%); and increased for both groups with celiprolol (5 vs 6%). Similar trends were observed with LDL cholesterol and the total/HDL cholesterol ratio. It is concluded that early noncardioselective beta blockers such as propranolol have significant dyslipidemic effects in both smokers and nonsmokers. Cardioselective drugs such as atenolol and metoprolol, or drugs with partial agonist activity such as pindolol, have variable effects. Celiprolol, a new, highly cardioselective beta 1 blocker with partial beta 2 agonist activity and vasodilatory properties, has favorable effects on lipids and minimizes the dyslipidemic effects associated with smoking.

Effects of pravastatin on thoracic aortic atherosclerosis in patients with heterozygous familial hypercholesterolemia.

Data regarding the effects of plasma lipid lowering on the evolution of thoracic aortic atherosclerosis (TAA) are scarce. In this study, we performed transesophageal echocardiography to characterize TAA in 16 newly diagnosed patients with heterozygous familial hypercholesterolemia and to follow its evolution after 2 years of statin treatment. TAA was graded as follows: grade I = normal intima; grade II = increased intimal echo density without thickening; grade IIIA = increased intimal echo density with single atheromatous plaque < or = 3 mm; grade IIIB = multiple plaques < or = 3mm; grade IV = > or = 1 plaque >3 mm; and grade V = mobile or ulcerated plaques. Baseline aortic intimal morphology was grade I in one patient, grade II in 4, grade IIIA in 6, grade IIIB in 3, and grade IV in 2 patients. Hypolipidemic treatment resulted in significant reductions in plasma total cholesterol and low-density lipoprotein (LDL) cholesterol. Follow-up aortic morphology was grade I in 5 patients, grade II in 2, grade IIIA in 3, grade IIIB in 3, and grade IV in 3 patients. TAA remained stable in 7 patients, progressed in 3, and regressed in 6 patients. TAA evolved in a uniform manner in the ascending aorta, aortic arch, and descending aorta. Patients with TAA regression were younger (39+/-14 vs 52+/-8 years, p=0.038) and had a greater decrease in plasma LDL cholesterol as a result of treatment (138+/-56 vs 73+/-55 mg/dl, p=0.036) than patients with TAA stability or progression. These observations support the hypothesis that hypolipidemic treatment may favorably affect the course of TAA in patients with heterozygous familial hypercholesterolemia.

Microalbuminuria is associated with abnormal thoracic aortic mechanics in essential hypertension.

In a population of 162 patients with currently untreated essential hypertension, those with microalbuminuria (n = 75) had significantly impaired elastic properties of the proximal ascending thoracic aorta compared with their normoalbuminuric counterparts (n = 87), whereas urinary albumin excretion was a significant predictor of aortic mechanics in the entire population. Impaired aortic mechanics in microalbuminuric hypertensives were not fully accounted for by clustering of classic risk factors for atherosclerosis, and constitute a finding that may entail additional long-term cardiovascular risk in this subgroup of patients.

Regression of left ventricular hypertrophy with isradipine antihypertensive therapy.

To assess left ventricular (LV) structural and functional changes, 45 hypertensive patients were studied by echocardiography after 2 weeks of placebo and 6 months of isradipine monotherapy. Although LV cavity size did not change, LV wall thickness decreased dramatically (P < .0001), producing a significant decrease in LV mass index (from 158 g/m2 to 136 g/m2; P < .0001). In addition, LV fractional shortening (FS) did not change (1.2%; P = NS) whereas the cardiac index increased (6.4%; P = .0007) due to a modest tachycardia accompanied by a reduction in total peripheral resistance (-22.1%; P < .0001). The magnitude of the reduction of LV mass was related to the degree of FS increase (r = -0.70; P < .0001), an indication of beneficial LV remodeling. It can be concluded that isradipine antihypertensive therapy leads to regression of LV hypertrophy without depression of LV pump function.

The effect of iron overload in the hearts of patients with beta-thalassemia.

BACKGROUND AND HYPOTHESIS: An important complication of beta-thalassemia is iron deposition in cardiac tissues resulting in fibrosis and dysfunction. Our aim was the investigation of the possible clinical effect of iron loading in the heart of patients with beta-thalassemia prior to the appearance of symptoms of depressed systolic function. METHODS: Thirty-five patients with beta-thalassemia, of whom 24 had the major type (Group 1) and 11 had the intermedia type (Group 2) were studied. Eleven age- and gender-matched controls were also studied (Group 3). All patients were evaluated echocardiographically and were shown to have normal left ventricular systolic function and dimensions. Serum ferritin, atrial natriuretic peptide (ANP), left atrial diameter (LAD), peak early mitral inflow velocity (E), peak late mitral inflow velocity (A), E/A ratio, deceleration time of the mitral inflow E wave (DT), and isovolumic relaxation time (IVRT) were measured. RESULTS: Univariate analysis showed that both groups of patients had similarly increased LAD and ANP plasma levels. Group 1 had a higher E/A ratio (2.27 +/- 0.88) SS than Group 2 (1.69 +/- 0.47, p = 0.05) and Group 3 (1.50 +/- 0.38, p = 0.01). Serum ferritin was significantly higher in Group 1 (3.526 +/- 0.352) than in Group 2 (2.808 +/- 0.288, p < 10(-5) and Group 3 (2.139 +/- 0.124, p < 10(-5). Multivariate analysis showed that ANP is a factor that is affected by the LAD and E/A ratio and that serum ferritin levels affect the LAD and E/A ratio. CONCLUSIONS: Although LAD and ANP levels are increased in patients with beta-thalassemia, the increased serum ferritin levels of patients seem to affect left atrial size and E/A ratio. ANP secretion is consecutively affected by these factors.

Left ventricular hypertrophy regression and function changes with ketanserin in elderly hypertensives.

Ketanserin is a serotonin antagonist with age-related antihypertensive efficacy. Its effects on left ventricular (LV) function and hypertrophy have not been adequately reported. We studied noninvasively 54 elderly hypertensives before and 6 months after ketanserin monotherapy. Mean blood pressure was controlled (174/101 to 145/86 mmHg, p less than 0.0001) with no heart rate changes. LV dimensions and volumes remained unchanged, as did all LV ejection indices, thus preserving LV output (p = ns). Total peripheral resistances fell (from means of 1986 to 1615 dynes, cm.s-5, p less than 0.0001), as did LV systolic wall stresses. Mean LV mass was reduced (248 to 237 g, p less than 0.0001), mainly due to interventricular septum thinning (11.8 to 11.1 mm, p less than 0.0001), resulting in a decrease in mean LV cross-sectional area (21.3 to 20.5 cm2, p less than 0.0001) and mass/volume ratio (2.14 to 2.01 p = 0.0001). Thus, LV hypertrophy regression did not affect contractility (LV mass index relation to stress/end-systolic volume index, r = -0.558 before and r = -0.564 after ketanserin therapy). It is concluded that ketanserin is an effective antihypertensive agent in the elderly that reduces LV hypertrophy indices and maintains cardiac output, with no concomitant burdening on LV hemodynamics.

Differentiation of beta-blocker effects on serum lipids and apolipoproteins in hypertensive patients with normolipidaemic or dyslipidaemic profiles.

To evaluate the differential effects of beta-blockers on serum lipids and apolipoproteins in normolipidaemic and dyslipidaemic hypertensives, 330 patients with mild to moderate essential hypertension were studied 1 month after placebo therapy and 6 months after monotherapy with propranolol (n = 53), atenolol (n = 66), metoprolol (n = 58), pindolol (n = 53), or celiprolol (n = 100). Serum total cholesterol, triglycerides, high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), and apolipoproteins (Apo) A1 and B were measured at baseline and study end. A total of 136 (41.2%) patients were considered normolipidaemic (pretreatment LDL-C < 160 mg.dl-1) and 194 (58.8%) were considered dyslipidaemic (LDL-C > 160 mg.dl-1). Changes in total cholesterol differed between normolipidaemics and dyslipidaemics with propranolol (+13% in normolipidaemics vs -0.5% in dyslipidaemics, P < 0.001), atenolol (+7% vs -2%, P = 0.01), metoprolol (+9% vs -4%, P0.0006), pindolol (+8% vs -9%, P < 0.001), and celiprolol (-1% vs -13%, P = 0.002). HDL-C differed less, with propranolol (-18% vs -13%), atenolol (-6% vs -2%), metoprolol (-2% vs -6%), pindolol (+4% vs +1%), and celiprolol (+9% vs +4%); none of these changes between normolipidaemic and dyslipidaemic patients were statistically significant. LDL-C changes differed the most, with propranolol (+35% vs -1%, P < 0.0001), atenolol (+15% vs -4%, P = 0.001), metoprolol (+12% vs -6%, P = 0.004), pindolol (+12% vs -13%, P < 0.0001), and celiprolol (+3% vs -16%, P = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of ketanserin and celiprolol on regression of left ventricular hypertrophy in older hypertensive patients.

The effects of ketanserin, a specific serotonin2-receptor agonist, and celiprolol, a new, highly cardioselective beta 1 blocker with partial beta 2 agonist activity and peripheral vasodilating properties, on left ventricular (LV) structure and function were assessed in 60 older hypertensive patients (greater than 55 years) with clinical LV hypertrophy (LV mass index greater than 130 g/m2). The patients were studied using echocardiography after 1 month of placebo treatment, and 6 and 18 months of monotherapy with active drug. Ketanserin and celiprolol lowered blood pressure to normal levels. Heart rate did not change with ketanserin and fell moderately (-5%) with celiprolol (p less than .001). Regression of LV hypertrophy was achieved with the use of either medication (p less than .0001), although the magnitude of reduction in LV mass was greater with celiprolol at both 6 months (-10% vs -5%, p = .001) and 18 months (-13% vs -7%, p = .002). While LV volume did not change with either drug, celiprolol tended to decrease it, resulting in a 5% reduction in cardiac index (p = .01), which was associated with mild bradycardia. Ketanserin did not change LV ejection fraction, whereas celiprolol caused a slight (1.5%) long-term improvement (p = .003). Systolic wall stress and total peripheral resistance decreased with both agents (p less than .01), with no between-group differences. In conclusion, anti-hypertensive treatment of older persons with ketanserin or celiprolol achieves regression of LV hypertrophy without associated deleterious effects on LV function.

Assessment of accuracy of the Doppler pressure half-time method in the estimation of the mitral valve area immediately after balloon mitral valvuloplasty.

AIM: The reliability of Doppler echocardiography in determining the mitral valve area after balloon mitral valvuloplasty has been questioned, as discrepancies were noted between measurements obtained by the pressure half-time method and those derived haemodynamically, immediately following completion of the procedure. Recent investigations, however, have indicated that these discrepancies may be attributable to the over-estimation of the mitral valve area by haemodynamic measurements, caused by the presence of the iatrogenic atrial septal defect complicating transseptal catheterization. The aim of the present study was to further test this hypothesis. METHODS AND RESULTS: Measurements of the mitral valve area by the Doppler pressure half-time method and the Gorlin formula were obtained and compared in 238 consecutive patients before and immediately after retrograde non-transseptal balloon mitral valvuloplasty, which does not involve puncture and/or dilatation of the inter-atrial septum. No significant difference was found between Doppler- and Gorlin-derived measurements, neither before (1.04 +/- 0.23 vs 1.03 +/- 0.23 cm2, P = ns) nor immediately after (2.14 +/- 0.47 vs 2.12 +/- 0.49 cm2, P = ns) valvuloplasty. Linear regression analysis demonstrated a high degree of correlation between Doppler and Gorlin measurements before (r = 0.778) and after (r = 0.886) the procedure. Good agreement was confirmed by the Bland-Altman method. CONCLUSION: Doppler echocardiography yields accurate measurements of the mitral valve area immediately after retrograde non-transseptal balloon mitral valvuloplasty. This finding supports the hypothesis that the creation of an iatrogenic atrial septal defect during transseptal catheterization may contribute to the poor agreement between Doppler and Gorlin data after balloon mitral valvuloplasty.