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Biomedical subjects

Carlos A Morillo

Publications and source records attributed to Carlos A Morillo.

At least 19 recordsLinked to original sources

CHARITY: Chagas cardiomyopathy bisoprolol intervention study: a randomized double-blind placebo force-titration controlled study with Bisoprolol in patients with chronic heart failure secondary to Chagas cardiomyopathy [NCT00323973].

BACKGROUND: Chagas' disease is the major cause of disability secondary to tropical diseases in young adults from Latin America, and around 20 million people are currently infected by T. cruzi. Heart failure due to Chagas cardiomyopathy is the main clinical presentation in Colombia. Heart failure due to Chagas' disease may respond to digoxin, diuretics and vasodilator therapy. Beta-adrenoreceptor antagonism seems to protect against the increased risk of cardiac arrhythmia and sudden death due to chronic sympathetic stimulation. The aim of this study is to evaluate the effects of the selective beta-adrenergic receptor blocker Bisoprolol on cardiovascular mortality, hospital readmission due to progressive heart failure and functional status in patients with heart failure secondary to Chagas' cardiomyopathy. METHODS/DESIGN: A cohort of 500 T. cruzi seropositive patients (250 per arm) will be selected from several institutions in Colombia. During the pretreatment period an initial evaluation visit will be scheduled in which participants will sign consent forms and baseline measurements and tests will be conducted including blood pressure measurements, twelve-lead ECG and left ventricular ejection fraction assessment by 2D echocardiography. Quality of life questionnaire will be performed two weeks apart during baseline examination using the "Minnesota living with heart failure" questionnaire. A minimum of two 6 minutes corridor walk test once a week over a two-week period will be performed to measure functional class. During the treatment period patients will be randomly assigned to receive Bisoprolol or placebo, initially taking a total daily dose of 2.5 mgrs qd. The dose will be increased every two weeks to 5, 7.5 and 10 mgrs qd (maximum maintenance dose). Follow-up assessment will include clinical check-up, and blood collection for future measurements of inflammatory reactants and markers. Quality of life measurements will be obtained at six months. This study will allow us to explore the effect of beta-blockers in chagas' cardiomyopathy.

Journal Article↗

Stroke prevention in patients with atrial fibrillation: the diagnosis and management of hypertension by specialists.

BACKGROUND: Hypertension is common in patients with atrial fibrillation (AF) and is an important cause of stroke. OBJECTIVES: To determine how effectively hypertension is managed among specialist-treated outpatients with AF. METHODS: Investigators reviewed the charts of patients with a diagnosis of AF cared for by medical specialists to determine the change in blood pressure, patterns of antihypertensive drug use and the role of the specialist in the management of hypertension. RESULTS: Of 209 patients with AF, 118 had a history of hypertension or an office blood pressure greater than 140/90 mmHg. Blood pressure was measured at 73% of all visits. Hypertension was identified as an important problem in 57% of patients and antihypertensive therapy was either initiated or suggested in 77%. One year after the initial specialist visit, systolic blood pressure was significantly lower (140+/-20 mmHg at one year versus 148+/-23 mmHg initially; P=0.015); however, there was no change in diastolic blood pressure (80+/-12 mmHg at one year versus 81+/-16 mmHg initially; P=0.602) and only 50% of patients had a blood pressure less than 140/90 mmHg. In contrast, the percentage of patients receiving warfarin increased from 46% to 78% (P=0.0001). CONCLUSIONS: In patients treated by specialists for AF, systolic blood pressure is significantly reduced during follow-up; however, 50% of patients continue to have suboptimal blood pressure control. In many patients, hypertension is not identified as an important comorbid illness and antihypertensive therapy is neither recommended nor initiated by the specialist. Greater specialist involvement in the identification and treatment of hypertension in patients with AF could lead to an important, additional reduction in stroke.

Aged↗

Acute vascular responses to isometric handgrip exercise and effects of training in persons medicated for hypertension.

Previous work from our laboratory demonstrated that isometric handgrip (IHG) training improved local, endothelium-dependent vasodilation in medicated hypertensives [McGowan CL (PhD Thesis), 2006; McGowan et al. Physiologist 47: 285, 2004]. We investigated whether changes in the capacity of smooth muscle to dilate (regardless of endothelial factors) influenced this training-induced change, and we examined the acute vascular responses to a single bout of IHG. Seventeen subjects performed four 2-min unilateral IHG contractions at 30% of maximal voluntary effort, three times a week for 8 wk. Pre- and posttraining, brachial artery flow-mediated dilation (FMD, an index of endothelium-dependent vasodilation) and nitroglycerin-mediated maximal vasodilation (an index of endothelium-independent vasodilation) were measured in the exercised arm by using ultrasound before and immediately after acute IHG exercise. IHG training resulted in improved resting brachial FMD (P < 0.01) and no change in nitroglycerin-mediated maximal vasodilation. Pre- and posttraining, brachial artery FMD decreased following an acute bout of IHG exercise (normalized to peak shear rate, pre-, before IHG exercise: 0.01 +/- 0.002, after IHG exercise: 0.008 +/- 0.002%/s(-1); post-, before IHG exercise: 0.020 +/- 0.003, after IHG exercise: 0.010 +/- 0.003%/s(-1); P < 0.01). Posttraining, resting brachial artery FMD improved yet nitroglycerin-mediated maximal vasodilation was unchanged in persons medicated for hypertension. This suggests that the training-induced improvements in the resting brachial artery FMD were not due to underlying changes in the forearm vasculature. Acute IHG exercise attenuated brachial artery FMD, and although this impairment may be interpreted as hazardous to medicated hypertensives with already dysfunctional endothelium, the effects appear transient as repeated exposure to the IHG stimulus improved resting endothelium-dependent vasodilation.

Aged↗

Central serotoninergic response to orthostatic challenge in patients with neurocardiogenic syncope.

AIMS: To determine whether central serotoninergic system activity is impaired by orthostatic challenge in patients with neurocardiogenic syncope (NCS). METHODS AND RESULTS: Thirty-five [mean age: 24 (SD): 6 years] patients with a clinical history of NCS and positive head-up tilt test and 35 age-matched healthy volunteers (CON = 25+/-5 years) with negative response were studied. Overnight dexamethasone suppression test (DST) (1.5 mg given at 11 p.m.) was performed to assess the sensitivity of the hypothalamic-pituitary-adrenal axis by measuring next day cortisol (microg/dL) at 8 a.m. and 4 p.m. Cardiac autonomic function, cortisol, and prolactin (ng/dL) were also determined at baseline supine (BAS) and after 5, 10, and 15 min of orthostatic stress (OS) at 60 degrees . No significant differences were observed in cortisol plasma levels after the DST: CON = 0.6+/-0.6 microg/dL vs. NCS = 0.6+/-0.5; P = 0.7. Cardiac autonomic function, cortisol, and prolactin responses were similar in both study groups (CON vs. NCS; P > 0.05) during BAS: cortisol = 8.6+/-4 vs.8.7+/-4 microg/dL and prolactin = 16.8+/-9 vs. 16.8+/-9 ng/dL; OS-5: cortisol = 8.7+/-5 vs. 8.5+/-4 microg/dL and prolactin = 16.9+/-9 vs. 15.8+/-9 ng/dL; OS-10: cortisol = 8.5+/-5 vs. 8.1+/-3 microg/dL; prolactin = 16.2+/-9 vs. 15.8+/-9 ng/dL, and OS-15: cortisol = 9.0+/-5 vs. 8.4+/-4 microg/dL; prolactin = 17.1+/-9 vs. 15.5+/-9 ng/dL. CONCLUSION: Central serotoninergic response during orthostatic challenge was not impaired in patients with recurrent NCS. These findings suggest that the activation of the hypothalamic-pituitary-adrenal axis is not altered in patients with recurrent NCS.

Adult↗

Age of first faint in patients with vasovagal syncope.

INTRODUCTION: Understanding whether vasovagal syncope is a lifelong disorder might shed insight into its physiology and affect management strategies. Accordingly, we determined the age of the first syncopal spell in adult patients who sought care for syncope. METHODS AND RESULTS: Patients were 42 +/- 18 years old with 64% women. They had had a median 8 syncope spells (interquartile range [IQR]: 4, 20) with a median frequency of 1.0 syncopal spells per year. The range of syncopal spells was 1-3,375, and the range of duration of history of syncope was 0.003-70 years. The first syncopal spell occurred at ages 0-81 in a skewed distribution, with a marked mode age of 13 years, a median age of 18 years (IQR 12, 37), and a mean age of 26 +/- 20 years. The distributions were statistically indistinguishable across countries (P = 0.50), among Canadian regions (P = 0.69), and between the studies (P = 0.49). The same modal values were seen in males and females, and in patients <40 and > or =40 years old. However, patients > or =40 years had median ages of onset older than patients <40 years (36 +/- 23 vs 17 +/- 8 years). Patients had a recalled history of syncopal spells of median duration of 10 years (IQR: 2, 23), with a range of 0.003-70 years. An age of onset <44 years was 86% accurate for vasovagal syncope. CONCLUSION: The most common age at which vasovagal syncope first presents is 13 years, and patients remain at risk of syncope for many years. Lifelong coping strategies may be desirable.

Adolescent↗

Prevention of atrial fibrillation with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: a meta-analysis.

OBJECTIVES: This study was designed to identify all randomized clinical trial data evaluating angiotensin-converting enzyme inhibitors or angiotensin receptor blockers for the prevention of atrial fibrillation (AF), to estimate the magnitude of this effect and to identify patient subgroups most likely to benefit. BACKGROUND: Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) reduce morbidity and mortality in patients with heart failure, vascular disease, and hypertension. Several reports suggest that they may also prevent the development of AF. METHODS: A systematic review of the literature was performed to identify all reports of the effect of ACEIs or ARBs on the development of AF. Eligible studies had to be randomized, controlled, parallel-design human trials of an ACEI or ARB that collected data on the development of AF. RESULTS: A total of 11 studies, which included 56,308 patients, were identified: 4 in heart failure, 3 in hypertension, 2 in patients following cardioversion for AF, and 2 in patients following myocardial infarction. Overall, ACEIs and ARBs reduced the relative risk of AF by 28% (95% confidence interval [CI] 15% to 40%, p = 0.0002). Reduction in AF was similar between the two classes of drugs (ACEI: 28%, p = 0.01; ARB: 29%, p = 0.00002) and was greatest in patients with heart failure (relative risk reduction [RRR] = 44%, p = 0.007). Overall, there was no significant reduction in AF in patients with hypertension (RRR = 12%, p = 0.4), although one trial found a significant 29% reduction in patients with left ventricular (LV) hypertrophy. In patients following cardioversion, there appears to be a large effect (48% RRR), but the confidence limits are wide (95% CI 21% to 65%). CONCLUSIONS: Both ACEIs and ARBs appear to be effective in the prevention of AF. This benefit appears to be limited to patients with systolic left ventricular dysfunction or LV hypertrophy. The use of these drugs following cardioversion appears promising but requires further study.

Angiotensin Receptor Antagonists↗

Impaired baroreflex gain in patients with inappropriate sinus tachycardia.

INTRODUCTION: The aim of this study was to determine the characteristics of heart rate variability (HRV), blood pressure variability (BPV), and baroreflex gain (BRG) at rest and during orthostatic stress in patients with clinical criteria of inappropriate sinus tachycardia (IST). METHODS AND RESULTS: Beat-to-beat HRV and BPV, measured by time- and frequency-domain methods, and noninvasive BRG, calculated by cross-spectral analysis, were obtained during 10 minutes both at rest and during the stabilization phase (5-15 min) of orthostatic stress at 60 degrees in 8 patients with clinical criteria of IST and 9 healthy volunteers (CON). IST patients had a higher resting mean heart rate (78.8 +/- 5.3 vs 58.5 +/- 4.2 beats/min, P=0.01) and mean blood pressure (90.4 +/- 2.4 vs 72.0 +/- 4.2 mmHg; P=0.002). RMSSD, pNN50m, and BRG were significantly reduced in IST patients at rest. BRG during orthostatic stress (7.2 +/- 0.8 vs 20.3 (2.4 ms/mmHg, P <0.01) was significantly reduced in IST patients. Delta BRG (-16.9%+/- 11 vs -50.1%+/- 5, P=0.02) was markedly blunted during orthostatic stress in IST patients. CONCLUSION: BRG was markedly impaired both at rest and during orthostatic stress in IST patients. This alteration may be responsible for the higher resting heart rate and mean blood pressures seen at rest and may facilitate tachycardia during orthostatic stress. A primary alteration in sinus node automaticity coupled with impaired BRG determines heart rate response to orthostatic stress in patients with IST.

Adaptation, Physiological↗

Role of the renin-angiotensin-aldosterone system in atrial fibrillation and cardiac remodeling.

PURPOSE OF REVIEW: This review summarizes recent clinical trial evidence showing a reduction in the development and recurrence of atrial fibrillation with angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor-blocking agents (ARBs). It then explores the possible mechanisms for this effect based on current animal models and limited human study. RECENT FINDINGS: Post hoc analyses of trials in patients with heart failure, hypertension, or myocardial infarction have observed reductions in atrial fibrillation among patients treated with ACE inhibitors or ARBs. Recent studies of these agents in animal models of atrial fibrillation suggest that they may prevent atrial fibrillation by reversing the cardiac structural and electrical changes, known as cardiac remodeling, that lead to the development of atrial fibrillation. This concept is also supported by two prospective studies showing that ACE inhibitors and ARBs prevent the recurrence of atrial fibrillation after electrical cardioversion. SUMMARY: Inhibition of the renin-angiotensin-aldosterone system is a novel concept for the treatment of atrial fibrillation that may target the underlying substrate of atrial fibrillation. Further human research is required to determine whether ACE inhibitors and ARBs prevent atrial fibrillation, and if so, whether this is a result of blood pressure lowering alone or a specific effect of these agents. Ongoing research will establish whether ACE inhibitors or ARBs have specific benefits in patients with atrial fibrillation.

Angiotensin Receptor Antagonists↗

The management of patients with carotid sinus syndrome: is pacing the answer?

Carotid sinus syndrome (CSS) is an under recognized cause of recurrent unexplained syncope and potentially of recurrent falls in the elderly. The mechanisms that lead to syncope in patients with CSS remain debated. However, evidence for both peripheral and central alterations have been recently reported. The diagnosis of CSS is challenging and a high clinical suspicion is usually needed to make the diagnosis. Clinical presentation may be typical and characterized by a clear association between accidental manipulation of the carotid sinus and the presentation of syncope. On the other hand, recurrent unexplained syncope and unexplained falls may be the clinical presentation of patients with CSS without a specific trigger. Carotid sinus hypersensitivity documented by carotid sinus massage (CSM) may be the only finding indicating the possibility of CSS as the cause of syncope. In older patients with recurrent unexplained syncope and a negative diagnostic work-up, carotid sinus massage both in the supine and upright positions is recommended. CSS may present primarily as a cardioinhibitory response or a true vasodepressor response. Therapy should address any underlying pathology if present, and be directed to either prevent cardioinhibition, vasodepression or both alterations. A variety of medical therapies have been used with unclear effects. No appropriately designed controlled clinical trials have been performed comparing pacing with medical therapy. Nonetheless, available information indicates that pacing may have a strong beneficial effect and prevents recurrence of syncope in patients with CSS. The present paper critically reviews the latest insights in the pathophysiology, diagnosis and management of CSS.

Cardiac Pacing, Artificial↗

Congestive heart failure in Latin America: the next epidemic.

Coronary artery disease is the main cause of congestive heart failure (CHF) in all populations. Latin American countries (LAC) are undergoing the first phase of an epidemic of coronary artery disease that probably will lead to an increased incidence of CHF. The progressive implementation of successful interventions, such as early reperfusion and rehabilitation programs, should increase the survival of patients with acute myocardial infarction and the population at high risk of CHF. The increasing prevalence of risk factors, such as diabetes, hypertension, and obesity, and the ageing of the population may also contribute to a rising incidence of CHF in LAC. Moreover, infectious diseases such as Chagas disease and rheumatic heart disease, known causes of CHF, are still frequent in this population and additionally contribute to the incidence of CHF. If timely preventive interventions are not implemented, CHF could become one of the main contributors to the burden of morbidity, mortality, and health costs in LAC. Properly conducted clinical and epidemiologic studies are needed to identify, implement, and evaluate preventive strategies that are likely to succeed within the specific context of LAC.

Adolescent↗

Cardiovascular autonomic function testing in asymptomatic T. cruzi carriers: a sensitive method to identify subclinical Chagas' disease.

BACKGROUND: Although impaired cardio-vagal response characterizes full-blown Chagas' disease, this feature among otherwise healthy T. cruzi serology carriers (SERO[+]) requires confirmation. The purpose of this study was to determine whether abnormal cardio-vagal responses were different among SERO[+] subjects with varying ECG alterations. METHODS: We assessed cardio-vagal reflex response in 57 randomly selected healthy blood donors (36 SERO[+], 15 with ECG rhythm/conduction abnormalities). The following cardiac autonomic tests were performed: (1) short-term heart rate variability (HRV), (2) Deep breathing test (DBT), (3) cold face test, (4) cold pressor test (CPT), (5) Valsalva maneuver, and (6) baroreflex sensitivity after administration of nitroprusside (BRS-NTP) and phenylephrine (BRS-PNP). RESULTS: Overall, SERO[+] subjects had 161/324 (49.7%) abnormal responses, compared to 41/189 (21.7%) in SERO[-] (p<0.001). Similar rates were found in SERO[+] according to ECG status (68/135, 50.4% in ECG[+] and 93/189, 49.2% in ECG[-], p=0.836). Covariate-adjusted pooled odd ratios (95%CI) for abnormal responses compared to SERO[-] were: 2.73 (1.71-4.35) for SERO[+], and 2.63 (1.63-4.34) for SERO[+]/ECG[-] (p<0.001). BRS-NTP, CPT and DBT individually showed significant differences between SERO[-] and SERO[+] groups. Conversely, ECG changes among SERO[+] were not associated with a significant excess of autonomic abnormality either overall (OR=1.09, 95%CI: 0.67-1.78, p=0.719) or by any individual test. CONCLUSIONS: Early cardio-vagal dysfunction was documented in SERO[+] subjects regardless of ECG status. Cardiac autonomic evaluation may be useful for identification of subclinical disease in SERO[+] subjects.

Adult↗