Sara Abram

Left atrial enlargement in essential hypertension: Role in the assessment of subclinical hypertensive heart disease

Abstract Background. Arterial hypertension is a common cause of cardiac organ damage, inducing morphofunctional modifications involving left chambers. This is a retrospective study: it was designed to evaluate the additive clinical value of left atrial enlargement (LAe) assessment in the evaluation of cardiac organ damage. Methods. A total of 814 (67% male; aged 50.7 ± 12 years, mean ± SD) essential hypertensive subjects underwent routinely to a complete and extensive clinical and echocardiographic evaluation. Left ventricular morphology, systolic and diastolic function and left atrial dimension (LAD; linear and volumetric) were evaluated. Results. Prevalence of LAe varied between 6.2% and 52.1%, depending on the chosen criteria (left atrial diameter indexed for body surface area (BSA) vs left atrial volume (LAV) indexed for BSA – LAVi). LAVi showed to be the most sensitive parameter in order to detect it (sensitivity 96%, specificity 100%). Left ventricular hypertrophy (LVH) was present in about one fifth of our population (14% and 26%, considering indexation for BSA and for height2.7). Concentric remodelling (CR) was present in 27–35% of cases considering left ventricular mass indexation for BSA and for height2.7, respectively. In one quarter of our population, LAe was the only echocardiographic sign of hypertension, independent of LVH and CR. Conclusions. LAV evaluation in hypertensive population can contribute to the identification of subjects affected by hypertensive heart disease other than the conventionally evaluated terms (LVH and CR).

Anti-hypertensive drugs and left ventricular hypertrophy: a clinical update.

Structural remodelling of the heart, known as left ventricular hypertrophy (LVH), is a consequence of systemic hypertension, and is associated with an increased risk of cardiovascular morbidity and mortality. Therefore, particular attention should be paid to the identification, prevention and treatment of this condition in hypertensive patients. LVH seems to benefit from all classes of anti-hypertensive drugs; however, antagonists of the renin–angiotensin–aldosterone system (RAAS) have demonstrated an additional benefit in the inhibition and reversal of myocardial interstitial fibrosis. Nevertheless, in evaluating the degree of arterial hypertension and organ damage, many neuro-hormonal systems are involved, primarily the sympathetic nervous system, thereby explaining the use of different classes of anti-hypertensive drugs to prevent or reduce LVH. The RAAS antagonists are actually the recommended anti-hypertensive agents to prevent organ damage in hypertensive subjects or in hypertensives with evidence of LVH to reduce cardiovascular mortality and morbidity.

Efficacy of antihypertensive treatment based on plasma renin activity: An open label observational study

Abstract Background. We investigated the extent of blood pressure (BP) reduction and control (<140/90 mmHg) in patients treated with appropriate or inappropriate drugs according to their plasma renin activity (PRA) level (natriuretic drugs and renin–angiotensin system blockers for low-renin and high-renin hypertension, respectively). Patients and methods. One hundred and seventy Caucasian untreated hypertensive patients (61 females), aged 18–70 years, participated to the study. Patients with secondary hypertension, diabetes or established cardiovascular or renal disease were excluded. The physician prescribed an antihypertensive monotherapy chosen among all drug classes, unaware of patients PRA levels. We compared effect of an inappropriate or appropriate drug, evaluating BP values after a month of treatment. Results. Rate of BP control was not significantly higher in patients treated with an appropriate drug than the others (38% vs 29%, p=0.24). However, in a regression analysis, final diastolic BP (DBP) was lower in subjects treated with an appropriate drug (β=−2.84, p=0.03). Conclusions. The present study does not clearly support the use of PRA in a general population of hypertensive patients to optimize BP control. However, the greater efficacy of a drug appropriate to PRA in reducing DBP may be clinically helpful in young hypertensive patients. Future studies are warranted to evaluate if PRA determination enhances the therapeutic success in patients with predominantly high values of DBP.

Echocardiographic Abnormalities in the Assessment of Cardiac Organ Damage in Never-Treated Hypertensive Patients

Hypertension-related cardiac organ damage, other than left ventricular (LV) hypertrophy (LVH), has been described: in particular, concentric remodeling, LV diastolic dysfunction (DD), and left atrial (LA) enlargement are significantly associated with cardiovascular morbility and mortality in different populations. This study evaluated the prevalence of these latter morphofunctional abnormalities, in never-treated essential hypertensive patients and the role of such a serial assessment of hypertensive cardiac damage in improving cardiovascular risk stratification in these patients. A total of 100 never-treated essential hypertensive subjects underwent a complete clinical and echocardiographic evaluation. Left ventricular morphology, systolic and diastolic function, and LA dimension (linear and volume) were evaluated by echocardiography. Left ventricular hypertrophy was present in 14% of the patients, whereas concentric remodeling was present in 25% of the subjects. Among patients free from LV morphology abnormalities, the most frequent abnormality was LA enlargement (global prevalence 57%); the percentage of patients with at least one parameter consistent with DD was 22% in the entire population, but DD was present as the only cardiac abnormality in 1% of our patient. Left atrial volume indexed for body surface area was the most sensitive parameter in identifying hypertension-related cardiac modification. The global prevalence of cardiac alteration reached 73% in never-treated hypertensive patients. Left ventricular remodeling and LA enlargement evaluation may grant a better assessment of cardiac organ damage and cardiovascular risk stratification of hypertensive patients without evidence of LVH after routine examination.

Frequency, Predictors, and Implications of Abnormal Blood Pressure Responses During Dobutamine Stress EchocardiographyCLINICAL PERSPECTIVE

Background— It is not known whether abnormal blood pressure (BP) responses during dobutamine stress echocardiography (DSE) are associated with abnormal test results, nor if such results indicate obstructive coronary artery disease (CAD). We sought to define the frequency of abnormal BP responses during DSE and their impact on accuracy of test results. Methods and Results— We studied 21 949 patients who underwent DSE at Mayo Clinic, Rochester, MN, grouped by peak systolic BP achieved during the test. We also analyzed a subgroup who underwent coronary angiography within 30 days after positive DSE. The positive predictive value of DSE was calculated for each BP group. Patients with hypertensive response (n=1905; 9%) were more likely to have positive DSE than those with normal (n=19 770; 90%) or hypotensive (n=274; 1%) BP responses (32% versus 21% versus 23%, respectively; P<0.0001). Angiography, performed in 1126 patients, showed obstructive CAD (≥50% stenosis) in 814 patients and severe CAD (≥70% stenosis) in 708 patients. Positive predictive value of DSE was similar for patients who had hypertensive and normal BP responses (69% versus 73%; P=0.3), considering 50% stenosis cut point. The proportion of severe CAD (≥70% stenosis) was lower in patients who had hypertensive response compared with those who had normal BP response (54% versus 65%; P=0.005). Conclusions— Patients with hypertensive response during DSE are more likely to have stress-induced myocardial ischemia compared with those with normal or hypotensive BP responses but are not more likely to have false-positive DSE results. They are, however, less likely to have higher grade or multivessel CAD.

Aldosterone inhibition in patients with heart failure with preserved ejection fraction.

Aldosterone Inhibition in Patients With Heart Failure With Preserved Ejection Fraction To the Editor The Aldosterone Receptor Blockade in Diastolic Heart Failure (Aldo-DHF) study1 tested the hypothesis that aldosterone inhibition with spironolactone would result in improvement in maximum exercise capacity (peak V̇O2) or diastolic function (E/e′), each a co-primary end point. Whereas resting E/e′ was reduced by spironolactone, exercise capacity was not. The method of patient selection may have contributed to a false-negative result. We believe that this study illustrates the fundamental problems with the current concept of heart failure (HF) with preserved ejection fraction (EF) and, in particular, the role of exercise in this syndrome. The definition of HF with preserved EF used by the investigators relied on the presence of breathlessness (New York Heart Association [NYHA] class >II), a preserved EF (>50%), and evidence of resting diastolic dysfunction (grade ≥1). Objective evidence of exercise limitation was necessary at baseline (via cardiopulmonary exercise testing) and resting spirometry was performed as a means to exclude those with respiratory limitation. Approximately half of the patients met diagnostic criteria of the European Society for Cardiology for HF with preserved EF, although the initiation of this study preceded the publication of these guidelines.2 Even though mean baseline peak V̇O2 (16.4 mL/min/kg) indicated significant exercise limitation, the mean expired volume per unit time/volume of expired carbon dioxide (V̇E/ V̇CO2) slope was 30.3. This implies that exercise limitation was not primarily cardiac in origin in approximately half of the patients. The V̇E/V̇CO2 slope has physiological, diagnostic, and prognostic implications3; a value of less than 30 is considered normal without adjustment for age and sex, whereas patients with HF typically far exceed this threshold. In this study, the normal mean V̇E/V̇CO2 slope suggests that many of these patients may have been primarily deconditioned and that pathophysiological heterogeneity may have been a major confounder. Heart failure with preserved EF should be considered a disorder in which therapeutic efficacy will primarily be seen in functional capacity. Phase 2 mechanistic trials are therefore likely to continue to use ergometric end points. However, the full physiological potential of cardiopulmonary exercise testing should be used to ensure a cardiac origin of limitation,4 thus validating the diagnosis of HF with preserved EF and increasing study power. In contrast, current guidelines2 emphasize resting echocardiographic indices, which are an insufficient basis on which to attribute a cardiac origin to dyspnea. If these fundamental issues are not addressed in trial methods, we believe negative findings will continue to predominate.