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Biomedical subjects

Peter Hanrath

Publications and source records attributed to Peter Hanrath.

At least 91 records · Page 5Linked to original sources
PubMed2003

The L-type Ca2+-channel subunits alpha1C and beta2 are not downregulated in atrial myocardium of patients with chronic atrial fibrillation.

OBJECTIVE: Electrical remodeling as well as atrial contractile dysfunction after the conversion of atrial fibrillation (AF) to sinus rhythm (SR) are mainly caused by a reduction of the inward L-type Ca(2+) current (I(CaL)). We investigated whether the expression of L-type Ca2+-channel subunits was reduced in atrial myocardium of AF patients. METHODS: Right atrial appendages were obtained from patients undergoing coronary artery bypass graft surgery (CAD, n = 35) or mitral valve surgery (MVD, n = 37). Seventeen of the CAD patients and 18 of the MVD patients were in chronic (>3 months) AF, whereas the others were in SR. The protein expression of the L-type Ca2+-channel subunits alpha1C and beta2 was quantified by western blot analysis. Furthermore, we measured the density of dihydropyridine (DHP)-binding sites of the L-type Ca2+ channel using 3H-PN220-100 as radioligand. RESULTS: Surprisingly, the alpha1C and the beta2-subunit expression was not altered in atrial myocardium of AF patients. Also, the DHP-binding site density was unchanged. CONCLUSION: The protein expression of the L-type Ca2+-channel subunits alpha1C or beta2 is not reduced in atrial myocardium of AF patients. Therefore, the reduced I(CaL) might be due to downregulation of other accessory subunits (alpha2delta), expression of aberrant subunits, changes in channel trafficking or alterations in channel function.

Animals↗
PubMed2003

Multislice spiral computed tomography for the detection of coronary stent restenosis and patency.

BACKGROUND: Multislice spiral computed tomography (MSCT) has evolved as a new promising method for non-invasive visualization of the coronary arteries and detection of native coronary artery stenosis. We determined the value of MSCT to non-invasively detect significant in-stent restenosis after coronary artery stenting. METHODS: Twenty patients (age 56.3+/-8.6 years) were investigated by MSCT (4x1 mm cross-sections, 500 ms tube rotation, table feed 1.5 mm/rotation, intravenous contrast agent, retrospectively ECG-gated image reconstruction) at a mean interval of 9.6+/-4.2 months after coronary stent implantation. Results were compared with conventional quantitative coronary angiography (QCA). A total number of 32 stents were studied, four different stent types were evaluated. RESULTS: QCA showed in-stent restenosis >50% diameter stenosis in five (16%) stents. Using MSCT it was impossible in all stents, irrespective of stent type or diameter, to directly visualize the stent lumen due to partial volume effects and beam hardening. MSCT allowed the visualization of the coronary vessel proximal and distal to the stent. This allowed confirmation of stent patency in 18/18 cases and correct identification of total stent occlusion in two patients. CONCLUSIONS: MSCT allows no direct visualization of coronary in-stent restenosis, but it correctly differentiates between stent patency and stent occlusion. The reasons are mainly partial volume effects and beam hardening, which are induced by the stent material.

Coronary Angiography↗
PubMed2003

Ciprofloxacin-induced acute psychosis in a patient with multidrug-resistant tuberculosis.

Tuberculosis (TB) increasingly appears in a multidrug-resistant form (MDR-TB) in Europe, too. Treatment remains difficult due to various side effects of the multi-drug-regimens. Ciprofloxacin is widely used as one of the few TB-second-line drugs. We report on the course of a ciprofloxacin-induced acute psychosis in a patient with MDR(isoniazid, streptomycin)-TB which resolved after cessation of ciprofloxacin treatment and introduction of a novel oxazolidone. Careful treatment considerations particularly in patients with additional predisposing factors to neuropsychiatric symptoms are recommended in the potentially dangerous MDR-TB, thus creating an enormous therapeutic challenge.

Acute Disease↗
PubMed2003

Use of subcutaneous enoxaparin compared to intravenous heparin and oral phenprocoumon in the setting of cardioversion--the ACE study (Anticoagulation in Cardioversion using Enoxaparin).

The mode and duration of anticoagulation in the setting of cardioversion of atrial fibrillation-either with or without guidance by transesophageal echocardiography (TEE)-is still an unresolved issue. Oral anticoagulation with warfarin or phenprocoumon is frequently used but may be associated with an increased risk of bleeding complications or, conversely, episodes of undercoagulation. Moreover, it takes several days to reach full anticoagulation with oral compounds. This phase may be covered with intravenous heparin but this requires prolonged hospitalization. Low-molecular weight heparin is an attractive alternative as it not only provides a safe and predictable level of anticoagulation with few side effects but can also be administered safely on an outpatient basis. In addition, anticoagulation monitoring is usually unnecessary. The ACE study (Anticoagulation in Cardioversion using Enoxaparin) compared the safety and efficacy of subcutaneous enoxaparin with intravenous heparin/oral phenprocoumon before and after cardioversion (stratified to TEE guidance or no TEE guidance). This article summarizes the study rationale and design. The results will be published shortly.

Administration, Oral↗
PubMed2003

Dilatation of the pulmonary veins in atrial fibrillation: a transesophageal echocardiographic evaluation.

Ectopic beats originating from sleeves of atrial tissue within the pulmonary veins (PVs) can induce and sustain paroxysmal atrial fibrillation (AF). Left atrial stretch and dilatation favors the development of atrial ectopy and AF. Similarly, PV dilatation, if present, might trigger PV ectopy in patients with AF. This study was designed to evaluate whether PV dilatation is present in patients with nonfocal AF and whether the PV diameter correlates to the left atrial diameter (LAD). The diameters of the right superior (RSPV) and left superior PV (LSPV) were measured at the ostium and at a depth of 1 cm in 170 patients (AF, n = 75; sinus rhythm [SR], n = 95) using transesophageal echocardiography. The LAD was determined by transthoracic echocardiography. The diameters of the PVs were significantly larger in patients with AF than in patients with SR (LSPV(ostium): AF 13.6 +/- 3.5 mm vs SR 10.6 +/- 2.7 mm, P < 0.001; LSVP(1cm): AF 12.5 +/- 2.9 mm vs SR 10.2 +/- 2.5 mm, P < 0.001; RSPV(ostium): AF 13.9 +/- 3.5 mm vs SR 11.7 +/- 2.9 mm, P < 0.001; RSVP(1cm): AF 12.8 +/- 2.8 mm vs SR 10.6 +/- 2.6 mm, P < 0.05). Similarly, LAD was larger in patients with AF (44.7 +/- 7.7 mm) as compared to patients with SR (38.8 +/- 6.8 mm, P < 0.001). Neither for the SR nor the AF group did the PV size correlate to the LAD. AF is associated with a significant enlargement of the RSPV, LSPV, and LAD. There is no correlation between LAD and PV diameters. This raises the question whether PV dilatation in patients with AF is a cause or a consequence of AF and whether it may contribute to the development and perpetuation of AF.

Aged↗
PubMed2003

Quantitative assessment of left ventricular function with interactive real-time spiral and radial MR imaging.

An interactive real-time spiral gradient-echo and an interactive real-time radial steady-state free precession sequence were investigated for the quantitative assessment of left ventricular function. Data were acquired in 18 patients without electrocardiographic triggering and breath holding. With the interactive real-time spiral gradient-echo sequence, significant underestimation of endocardial and epicardial volumes was demonstrated; with the interactive real-time radial steady-state free precession sequence, excellent agreement was shown with standard cardiac-triggered segmented k-space breath-hold steady-state free precession MR imaging. Interactive real-time radial steady-state free precession imaging allows accurate quantitative assessment of left ventricular volumes.

Adult↗
PubMed2003

Cardioprotection by Carvedilol: antiapoptosis is independent of beta-adrenoceptor blockage in the rat heart.

BACKGROUND: Carvedilol, a beta-blocking agent with beta-blocking properties is now widely used for the treatment of congestive heart failure. In addition to its beta-adrenergic receptor blockage, antiapoptotic effects have been demonstrated in experimental animals. OBJECTIVE: The cardioprotective effects of carvedilol and its hydroxylated analogue BM-91.0228 were tested with regard to their infarct-limiting and antiapoptotic properties in an experimental infarct model in the rat heart. METHODS: Anesthetized rats were subjected to either 30 (groups 1 to 3) or 60 minutes (groups 4 to 6) of coronary artery occlusion followed by 30 minutes of reperfusion. Groups 1 and 4 served as the control; groups 2 and 5 received intravenous Carvedilol (1 mg/kg) and groups 3 and 6 received intravenous administration of BM-91.0228 (1 mg/kg), respectively, 5 minutes prior to coronary occlusion. Infarct sizes were measured by triphenyltetrazolium chloride staining. In situ visualization of apoptosis was measured by nick end labeling. RESULTS: Carvedilol reduced infarct size after 30 minutes of coronary occlusion compared to controls (8.7% +/- 2.7% versus 27.3% +/- 3.4%, P <.001), while BM-91.0228 showed no significant infarct size reduction (23.7% +/- 5.9%, NS). Neither Carvedilol (36.9% +/- 3.9%) nor BM-91.0228 (42.4% +/- 3.6%) reduced infarct size after 60 minutes of coronary occlusion compared to controls (47.7% +/- 3.9%, NS). Carvedilol reduced apoptosis after 30 minutes (4.9% +/- 1.3% versus 16.7% +/- 3.2%, P <.01) and after 60 minutes (11.7% +/- 1.8% versus 25.5% +/- 0.5%, P <.001) of coronary occlusion compared to controls. BM-91.0228 reduced apoptosis after 30 minutes (7.3% +/- 1.4% versus 16.7% +/- 3.2%, P <.01) and after 60 minutes (13.4% +/- 1.8% versus 25.5% +/- 0.5%, P <.001) of coronary occlusion compared to controls. CONCLUSION: Carvedilol is cardioprotective by preventing ischemia-perfusion-induced necrosis and apoptosis of cardiomyocytes. The antiapoptotic effects of Carvedilol are independent of its beta-adrenoceptor blocking effects, but its effects might be caused by antioxidant properties and by modulation of the signalling pathway.

Adrenergic beta-Antagonists↗
PubMed2002

Deposition of platelet RANTES triggering monocyte recruitment requires P-selectin and is involved in neointima formation after arterial injury.

BACKGROUND: Chemokines expressed on atherosclerotic endothelium or deposited by activated platelets have been implicated in monocyte recruitment during atherogenesis and restenosis. Although the involvement of P-selectin in these processes is evident from studies in knockout mice, it has not been elucidated whether delivery of platelet chemokines requires P-selectin, thus serving as a P-selectin-dependent effector function. METHODS AND RESULTS: Using immunofluorescence and laminar flow assays, we found that the deposition of the platelet-derived chemokine RANTES and monocyte arrest subsequently triggered by RANTES immobilized on inflamed endothelium are more efficient after preperfusion than after static preincubation of platelets and appear to depend on interactions of platelet but not endothelial P-selectin. This was revealed by the effects of P-selectin antibodies and comparison of P-selectin-deficient and wild-type platelets. Immunohistochemistry detected a substantial luminal expression of RANTES on neointimal lesions in wire-injured carotid arteries of apolipoprotein E (apoE)-deficient mice but not of mice with a combined deficiency in apoE and P-selectin (or platelet P-selectin). As assessed by histomorphometry, treatment of apoE-deficient mice with the RANTES receptor antagonist Met-RANTES markedly reduced neointimal plaque area and macrophage infiltration. CONCLUSIONS: Our data suggest that RANTES deposition and subsequent monocyte arrest are promoted by platelet P-selectin and involved in wire-induced intimal hyperplasia, and that blocking RANTES receptors attenuates neointima formation and macrophage infiltration. This mechanism represents an important component explaining the protection against neointimal growth in P-selectin-deficient mice and may represent a novel approach to the treatment of restenosis or atherosclerosis by the administration of chemokine receptor antagonists.

Animals↗
PubMed2002

Randomized comparison of success and adverse event rates and cost effectiveness of one long versus two short stents for treatment of long coronary narrowings.

Long stents of high flexibility and low profile have become widely available. Treatment of long coronary lesions by 1 long stent may require less interventional efforts and reduce the rate of restenosis due to a lack of overlapping stent segments. This study sought to evaluate the use of 1 long stent compared with 2 short stents for treatment of long coronary lesions. One-hundred twenty-four patients with a coronary lesion 20 to 40 mm in length, in a vessel 2.5 to 4.0 mm in diameter, were randomly assigned to treatment with 1 long stent (GFX II stents or S670 of 24, 30, or 40 mm lengths; n = 62) or 2 stents (GFX II or S670 stents, n = 62) of equal length. Procedural success, interventional costs, as well as long-term clinical and angiographic outcomes were evaluated. Lesion characteristics were similar for the 2 treatment groups. Stent placement was possible as assigned by randomization in 61 of 62 cases (98%) in the 1-long-stent group and 100% of cases in the 2-short-stents group. There was crossover to successful short-stent placement in 1 case. The in-hospital success rate was 97% for the 1-long-stent group and 98% for the 2-short-stents group. Acute angiographic results were similar for both groups after intervention. The angiographic restenosis rate at 6 months was 38.5% in the 1-long-stent group and 37.5% in the 2-short-stents group (p = 0.919). Intervention time was less, and the need for a contrast agent had a tendency to be lower in the long-stent group. Procedural costs were significantly less in the long-stent group. In conclusion, 1 long stent can be used with identical procedural success and adverse event rates as 2 short stents in long, atherosclerotic coronary lesions. The restenosis rate is not reduced by the use of 1 long stent compared with 2 stents. However, long stent placement is highly cost effective.

Aged↗
PubMed2002

brain natriuretic peptide levels predict functional capacity in patients with chronic heart failure.

OBJECTIVES: The goal of this study was to determine if brain natriuretic peptide (BNP) levels are associated with exercise capacity in patients with chronic heart failure (HF). BACKGROUND: Plasma levels of BNP are increased subject to the degree of systolic and diastolic left ventricular dysfunction in patients with chronic HF. Exercise testing is useful to assess functional capacity and prognosis in chronic HF. METHODS: We prospectively studied 70 consecutive patients with chronic HF (60.3 +/- 10.4 years, 51 men) referred for cardiopulmonary exercise testing. Resting BNP was obtained after 10 min of supine rest before symptom-limited bicycle exercise testing. RESULTS: In patients with chronic HF, BNP levels correlated with oxygen uptake (VO(2)), both at anaerobic threshold (VO(2)AT: r = -0.54, p < 0.001) and peak exercise (peak VO(2): r = -0.56, p < 0.001). Impairment of ventilatory efficiency (EqCO(2): r = 0.43, p < 0.001) and maximum exercise level (W % predicted: r = -0.44, p < 0.05) correlated less well with BNP. There was a significant inverse correlation between left ventricular ejection fraction and BNP (r = -0.50, p < 0.05). Brain natriuretic peptide discriminated well chronic HF patients with a peak VO(2) <10 ml/min/kg (area under the receiver operating characteristic [ROC] 0.93) or <14 ml/min/kg (area under the ROC 0.72). A BNP >316 pg/ml was associated with a risk ratio of 6.8 (95% confidence interval, 2.3 to 19.8) for a reduced exercise capacity with a peak VO(2) <14 ml/min/kg. CONCLUSIONS: Brain natriuretic peptide is clearly associated with exercise capacity in chronic HF. Brain natriuretic peptide levels show a significant correlation with the impairment of VO(2) at peak exercise and anaerobic threshold. Brain natriuretic peptide is able to differentiate between chronic HF patients with moderately and severely impaired exercise capacity.

Chronic Disease↗
PubMed2002

Vasopeptidase inhibition with omapatrilat in chronic heart failure: acute and long-term hemodynamic and neurohumoral effects.

OBJECTIVES: We investigated the acute and long-term hemodynamic and neurohumoral effects of the vasopeptidase inhibitor omapatrilat in human heart failure. BACKGROUND: Angiotensin-converting enzyme (ACE) inhibition constitutes a major advance in the treatment of chronic heart failure (CHF). Simultaneous inhibition of both neutral endopeptidase and ACE with omapatrilat may represent a new treatment strategy in CHF. METHODS: Three hundred and sixty-nine patients with symptomatic heart failure were randomized to double-blind treatment with omapatrilat (first 190 patients: 2.5 mg, 5 mg or 10 mg; last 179 patients: 2.5 mg, 20 mg or 40 mg once daily) for 12 weeks. RESULTS: Acutely, the 10 mg, 20 mg and 40 mg doses of omapatrilat produced greater reductions in pulmonary capillary wedge pressure (PCWP), systolic blood pressure (SBP) and systemic vascular resistance compared with 2.5 mg. Higher doses were associated with greater increases in vasodilator and natriuretic peptides, in addition to ACE inhibition. After 12 weeks, omapatrilat 20 mg and 40 mg showed greater falls from baseline in PCWP (40 mg: 0 h to 12 h average change -7.3 +/- 0.8 mm Hg) and SBP (40 mg: -11.7 +/- 1.7 mm Hg) than 2.5 mg (both p < 0.01 vs. 2.5 mg). The incidence of adverse experiences and patient withdrawal were similar in all groups. CONCLUSIONS: In CHF, the acute hemodynamic benefit seen with higher doses of omapatrilat was associated with increases in plasma vasodilator and natriuretic peptide levels in addition to ACE inhibition. After 12 weeks, the hemodynamic benefit was maintained. Omapatrilat may be a promising new agent in CHF.

Aged↗
PubMed2002

Relation of stent design and stent surface material to subsequent in-stent intimal hyperplasia in coronary arteries determined by intravascular ultrasound.

A variety of different stent designs and coatings have become available. This study sought to determine the impact of stent design and gold-coating of stents on intimal hyperplasia (IH) in human atherosclerotic coronary arteries in relation to known predictors of restenosis. Angiographic and intravascular ultrasound (IVUS) studies were performed at 6-month follow-up on 311 native coronary lesions of 311 patients treated with 99 Multi-Link stents, 74 InFlow steel stents, 73 InFlow gold-coated stents, 41 Palmaz-Schatz stents, 12 NIR steel stents, and 12 gold-coated NIR Royal stents. Lumen and stent cross-sectional area (CSA) were measured at 1-mm axial increments. Mean IH CSA (stent CSA - lumen CSA) and mean IH thickness were calculated and averaged over the total stent length. IVUS demonstrated different levels of IH for the 6 stents. Mean IH thickness ranged from 0.20 +/- 0.13 mm for Multi-Link stents to 0.43 +/- 0.14 mm for InFlow goal-coated stents (p <0.001). Multivariate analysis proved non-Multi-Link stent design (odds ratio 3.45, 95% confidence intervals 1.13 to 11.11, p <0.034) and gold coating (odds ratio 3.78, 95% confidence intervals 1.88 to 7.54, p <0.001) to be the only independent predictors of IH thickness >0.3 mm. In conclusion, stent design and surface material have an important impact on the IH response to stents implanted in human coronary arteries. However, the differences in IH thickness between the analyzed stents were relatively small compared with the absolute lumen dimensions.

Analysis of Variance↗
PubMed2002

Variants of the CYP11B2 gene predict response to therapy with candesartan.

In a prospective trial, patients with an elevated diastolic blood pressure (above 95 mm Hg) received high-dose (16 mg) or low-dose (8 mg) candesartan in addition to standardised medication. A positive response to treatment was defined as a diastolic blood pressure <85 mm Hg at follow-up. Genotyping for two candidate genes was performed in 116 patients. Genotypes of the CYP11B2 promotor polymorphism significantly predicted a positive response to treatment (CC: 67%; TC: 34%; TT: 21%; p=0.005).

Aged↗
PubMed2002

Activation of IP and EP(3) receptors alters cAMP-dependent cell migration.

Migration of vascular smooth cells from the media to the intima essentially contributes to neointima formation after percutaneous transluminal angioplasty and stent implantation. The stable prostacyclin mimetic iloprost has been shown to inhibit neointima formation in experimental restenosis, but it is currently unknown whether this may be caused by an antimigratory effect. Hence, the present study analyses (i) the influence of G(s)-coupled prostacyclin (IP) receptors on cell migration and (ii) verifies whether EP(3) receptors with opposite (i.e., G(i)) coupling may conversely stimulate cell migration. In a modified Boyden chamber model, it was shown that iloprost dose-dependently inhibits the migration of primary human arterial smooth muscle cells, which constitutively express the IP receptor. On the other hand, human arterial smooth muscle cell migration was stimulated by the EP(3) receptor agonist M&B 28.767. To independently study the effects of these receptors, IP or EP(3) receptors were stably overexpressed in chinese hamster ovary cells (CHO-IP and CHO-EP(3)). Chemotaxis of CHO cells transfected with G(s)-coupled IP receptors was concentration-dependently inhibited by iloprost (2-100 nM), while there was no effect of iloprost on mock-transfected CHO. By contrast, CHO-cells that overexpressed EP(3) receptors showed a significant, concentration dependent (1-100 nM) increase of cell migration in presence of the selective EP(3) agonist M&B 28.767. It is concluded that the prostacyclin mimetic iloprost inhibits vascular cell migration, which probably depends on a G(s)-mediated increase of intracellular cAMP. EP(3) receptors conversely stimulate CHO migration.

Animals↗
PubMed2002

Repeated assessment of coronary flow velocity pattern in patients with first acute myocardial infarction.

OBJECTIVES: The aim of this study was to evaluate the coronary blood flow velocity pattern immediately and 24 h after percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction (AMI) in relation to myocardial reperfusion and follow-up left ventricular (LV) function. BACKGROUND: Analysis of coronary blood flow velocity pattern after AMI may provide information about microvascular damage and the occurrence of a reperfusion injury. METHODS: Measurement of coronary blood flow velocity pattern was performed immediately after PTCA and after 24 h in 25 patients with first AMI using a Doppler guidewire. Measurements were related to reperfusion determined by intravenous myocardial contrast echocardiography (MCE) performed before PTCA and at 24 h and to LV function at four weeks. RESULTS: Using MCE, 13 patients showed reperfusion and 12 patients showed nonreperfusion. Compared with patients with reperfusion, patients with MCE nonreperfusion had a lower systolic peak flow velocity immediately after PTCA (10.0 +/- 0.3 cm/s vs. 19.3 +/- 0.8 cm/s, respectively) and after 24 h (12.3 +/- 0.4 cm/s vs. 21.3 +/- 0.1 cm/s, respectively, p = 0.0022), more frequent early systolic retrograde flow (6/12 vs. 0/13, p = 0.0052 immediately after PTCA and 24 h later) and a shorter diastolic deceleration time immediately after PTCA (483 +/- 6 ms vs. 737 +/- 0 ms, respectively) and after 24 h (551 +/- 9 ms vs. 823 +/- 2 ms, respectively, p = 0.0091). Similarly, patients with impaired LV function at four weeks had altered coronary flow pattern compared with patients with preserved function. The coronary flow velocity pattern showed a tendency for improvement after 24 h in the reperfusion and the nonreperfusion groups. CONCLUSIONS: The coronary flow velocity pattern immediately and 24 h after PTCA for AMI relates to myocardial perfusion determined by MCE and LV function at four weeks. The flow velocity pattern shows slight improvement during the first 24 h after revascularization, indicating the absence of a major reperfusion injury.

Aged↗
PubMed2002

Regression of left ventricular mass one year after aortic valve replacement for pure severe aortic stenosis.

The aim of the study was to quantify a 1-year change in left ventricular (LV) mass index (MI) and systolic LV function in 30 patients with pure severe aortic stenosis by means of serial 3-dimensional (3-D) echocardiography. To assess the completeness of LVMI regression after 1 year, we compared the postoperative mass of patients with mass values of 30 normotensive control subjects without a history of cardiac disease. Ejection fraction increased from 64 +/- 14% before surgery to 69 +/- 8% at follow-up (p = 0.067), and functional class improved from 2.9 +/- 0.5 to 1.4 +/- 0.5 (p <0.05), with improvement in each patient. During the same period, LVMI regressed by 23.4% (p <0.001). Postoperative LVMI was related to preoperative LVMI (r = 0.82; p <0.001) and baseline ejection fraction (r = -0.5; p = 0.009). LVMI regressed into the normal range in 64% of patients at follow-up. Patients achieving normal mass values did not differ with respect to patient gender, valve type, or valve size. Patients with reduced preoperative LV function had larger volumes (p <0.01), larger mass values (p <0.01), and a trend toward more mass regression (p = 0.062) than patients with normal preoperative function. Although ejection fraction improved after 1 year in all of these patients (p <0.03), they were less likely to achieve normal mass values at follow-up (p = 0.01). Regression of LVMI in patients with pure aortic stenosis is a positive event that occurs in each patient and that is associated with improvement in functional status. LVMI regressed into the normal range in most patients with normal preoperative function. Preoperative LV function, but not patient gender, valve type, or size, was related to normalization of LVMI at follow-up in this selected study population.

Aged↗