PubMed Health⌕ Search

Biomedical subjects

D Aristizabal

Publications and source records attributed to D Aristizabal.

9 recordsLinked to original sources
PubMed2001

Influence of setting on unattended respiratory monitoring in the sleep apnoea/hypopnoea syndrome.

The high demand for full polysomnography and the better quality of sleep at home are the main reasons for performing home sleep studies. Home respiratory monitoring has been evaluated in several studies, but the influence of setting on the results of unattended respiratory monitoring has not been assessed to date. Unattended monitoring of respiratory variables at home and in the sleep laboratory was conducted in 35 consecutive patients with suspected sleep apnoea/hypopnoea syndrome. Respiratory variables during sleep, rate of successful studies and patient preference were compared. The data acquisition failure rate was 2.8% in the sleep laboratory and 5.7% at home. The mean difference between apnoea/hypopnoea indices (AHI) obtained from home and laboratory studies was -0.21 +/- 8 (95% confidence interval 3.27-2.84). Using the method comparison approach of Bland and Altman, the limits of agreement of the mean difference between AHI home and AHI laboratory were -16.7 and 17.1. No difference was observed between the studies in time spent in different body positions. When patients were asked where they would prefer to repeat the sleep study, 53% replied at home, 28% in hospital and 19% showed no preference. It was concluded that the setting of unattended respiratory monitoring (home or sleep laboratory) influences neither the number of valid studies nor the results of the respiratory parameters measured; most patients, however, preferred home studies.

Adult↗
PubMed1996

Myocardial contrast echocardiography in human beings: correlation of resting perfusion defects to sestamibi single photon emission computed tomography.

The presence of myocardial perfusion abnormalities is generally accepted to suggest underlying coronary artery disease. In previous animal studies, myocardial contrast echocardiography (MCE) has been shown to be useful in delineating areas at risk after coronary occlusions. We sought to compare the presence or absence, size, and location of perfusion defects detected in human beings by MCE and sestamibi single photon emission computed tomography (SPECT). Regional wall motion was qualitatively assessed in the parasternal and apical views of a resting two-dimensional echocardiogram. Coronary angiography was performed in all patients and myocardial contrast echocardiography performed with 2 ml of intracoronary sonicated meglumine (Nycomed). A cine loop of the digitized contrast echocardiograms was used to analyze perfusion defects. Gated SPECT resting images in standard views were obtained after technetium 99m sestamibi (20 mCi) was administered. Visually perceived perfusion defects were established at 30% of maximal counts at end diastole. Perfusion defects by both techniques were planimetered, assigned to one of three perfusion artery territories, and expressed as a percentage of the perfusion territory studied. Comparison was made by linear regression analysis. Forty-one patients were studied. Perfusion defects were observed in 12 (29%) patients by MCE, 19 (46%) patients by SPECT, and 11 (27%) patients by both techniques. No perfusion defects were detected by MCE in 29 (70%) patients, by SPECT in 22 (53%) patients, or by either technique in 21 (51%) patients. The two techniques agreed in 78% of the patients. In 67 matching orthogonal views suitable for comparison between the two techniques, an 82% concordance for the presence or absence of defects was observed. The location of the defects matched in 86% of the cases. A significant correlation (p < 0.001; r = 0.62) between these techniques was observed in assessing the size of perfusion defects. In conclusion, our results suggest that MCE and sestamibi SPECT are comparable techniques for detecting severely underperfused myocardium in human beings.

Adult↗
PubMed1996

Investigative Concerns in Demonstrating Reduced Risk From Reversing Left Ventricular Hypertrophy.

BACKGROUND: To demonstrate reduced risk from reversing left ventricular hypertrophy (LVH) in hypertension, one must show that it is independent of blood pressure reduction. METHODS AND RESULTS: A feasibility study was conducted with 15 patients. The study employed 48-hour Holter recording, exercise treadmill (for ST-segment changes) and, as necessary, thallium scintigraphy and coronary angiography. All patients were treated for 3 months with quinapril (10 mg) and demonstrated decreased mean arterial pressure (125 +/- 3.1 vs 103 +/- 1.9 mmHg; P <.01) and left ventricular mass index (125 +/- 6.4 vs 104 +/- 4.9; P <.02) with preserved left ventricular function. There were no significant changes in these patients with moderate LVH in the incidence of arrhythmias; however, 4 of the 15 patients developed ST-segment changes prior to LVH reversal, and these changes did not recur in 3 patients following reversal of LVH or when pressure was allowed to rise. CONCLUSIONS: Ischemic changes, rather than development of arrhythmias, may be of greater value in demonstrating risk reduction with LVH reversal. Moreover, these preliminary data suggest pitfalls in demonstrating risk reduction after LVH reversal, indicating that more sensitive and adequate techniques are necessary to show risk reduction from LVH.

Journal Article↗
PubMed1994

Disparate structural effects on left and right ventricles by angiotensin-converting enzyme inhibitors and calcium antagonists in essential hypertension.

Reduced left ventricular (LV) mass and wall thicknesses with angiotensin-converting enzyme (ACE) inhibitors and calcium antagonists occur in essential hypertension. Experimental studies have shown that reduction in LV mass is related to hemodynamic as well as nonhemodynamic factors that may influence LV and also right ventricular (RV) structure. Sixty-eight patients with essential hypertension were studied echocardiographically 4 to 8 weeks after antihypertensive therapy was initiated. LV dimensions and wall thicknesses, as well as RV free wall thickness, were measured using 2-dimensionally guided techniques. Patients were divided in 2 groups: those receiving either ACE inhibitors or calcium antagonists. This short-term therapeutic period produced similar hemodynamic changes and reductions in LV mass in both groups. In these 2 groups of patients, we found opposite effects in RV free wall thickness. Thus, RV wall thickness increased from 0.44 +/- 0.02 to 0.56 +/- 0.02 cm (p < 0.01) after therapy in the calcium antagonist group, whereas no change was found in the ACE inhibitor group (0.36 +/- 0.04 vs 0.34 +/- 0.04). These structural changes suggest that ACE inhibitors and calcium antagonists produce dissimilar effects on cardiac cell growth and growth reversal, which may be mediated through different nonhemodynamic effects after short-term therapy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

Preserved cardiac performance with reduced left ventricular mass in conscious exercising spontaneously hypertensive rats.

OBJECTIVES: To investigate whether cardiovascular performance can be modified beneficially with left ventricular hypertrophy reversal and whether the associated sudden afterload increases may adversely affect overall cardiac performance. METHODS: We studied cardiovascular performance with thermodilution techniques at rest and during maximal treadmill exercise after 3 weeks' treatment with the angiotensin converting enzyme inhibitor quinapril (3 mg/kg per day) in 19 male spontaneously hypertensive rats (SHR) aged 20 weeks. RESULTS: Left ventricular mass was reduced significantly, without impairment of exercise performance, demonstrating that left ventricular hypertrophy reversal benefited or at least did not hinder cardiovascular adaptation to physiologic exercise in the SHR. Moreover, decreasing the afterload did not further improve the performance after the reversal of left ventricular hypertrophy.

Animals↗
PubMed1993

Left ventricular hypertrophy: should it be reduced?

Left ventricular hypertrophy (LVH) is a structural adaptation of the heart to sustained hypertension, serving to normalize increased wall stress. Recent clinical studies have indicated that LVH is a powerful pressure-independent risk factor for cardiovascular morbidity and mortality, particularly sudden death, acute myocardial infarction, and congestive failure. The pathophysiologic sequelae of LVH consist of reduced ventricular filling and contractility, ventricular dysrhythmias, and diminished coronary reserve or myocardial ischemia. LVH can be reduced by antihypertensive therapy, although not all drugs are equipotent in this regard. Angiotensin-converting enzyme (ACE) inhibition seems to be the most powerful monotherapeutic modality for reducing LVH. Recent studies have shown that such a reduction also improves the pathophysiologic sequelae of LVH and maintains left ventricular pump function. Although the reversal of these pathophysiologic events is encouraging, it remains unknown whether reducing LVH will ultimately decrease the excessive risk of sudden death, acute myocardial infarction, and congestive heart failure that has been associated with this disorder independently of arterial pressure.

Heart↗
PubMed1993

Reduction of left ventricular hypertrophy: how beneficial?

Left ventricular hypertrophy (LVH) can no longer be considered a compensatory adaptation of the heart serving to normalize the increased wall stress in hypertension. Recent studies have indicated that LVH is a powerful pressure-independent risk factor for cardiovascular morbidity and mortality. The pathophysiologic sequelae of LVH are reduced ventricular filling and contractility, ventricular dysrhythmias, and diminished coronary reserve or myocardial ischemia. Left ventricular hypertrophy can be reduced by antihypertensive therapy, although not all drugs are equipotent in this regard. Recent studies have shown that such a reduction also improves the pathophysiologic sequelae of LVH, that is, ventricular filling, coronary reserve, and ventricular dysrhythmias, and maintains left ventricular pump function. Although the reversal of these pathophysiologic findings is encouraging, it remains unknown whether a reduction of LVH will ultimately reduce the excessive risk of sudden death, acute myocardial infarction, and congestive heart failure that has been associated with this disorder independent of arterial pressure.

Calcium Channel Blockers↗
PubMedDate not supplied

Hypertension due to renal arterial disease.

Renal arterial disease occurs in 3-5% of patients with systemic hypertension. It is important to determine the type of lesion by arteriography to understand the natural history of the specific disease and to choose appropriate therapy. Some have questioned why arteriography should be performed if an operation or percutaneous transluminal renal angioplasty is not considered. One must keep in mind that if the arteriographic characteristics are known, the specific lesion and its course may be predicted, resulting in better management of the disease. In patients with a unilateral lesion angiotensin converting enzyme inhibitors are efficacious, but calcium antagonists may also be used. However, if therapy does not provide optimum control of blood pressure or the impairment of renal function progresses, then percutaneous transluminal renal angioplasty or surgery should be reconsidered.

Humans↗