Mild left ventricular hypertrophy in essential hypertension: is it really arrhythmogenic?

Left ventricular hypertrophy (LVH) has been associated with an increased incidence of ventricular arrhythmias and sudden cardiac death in hypertensive patients. However, it is not known whether this relationship exists in early asymptomatic hypertensives with mild LVH. We prospectively examined 100 consecutive patients with essential hypertension, 35 without and 65 with mild LVH on echocardiography. All underwent a detailed noninvasive arrhythmia work-up and were subsequently followed-up for 3 ± 1 years in an ambulatory hypertension clinic. None of the 12-lead electrocardiographic parameters examined differed between the two hypertensive groups. A similarly low incidence of simple forms of ventricular ectopy was present in both groups, whereas complex forms of ventricular ectopy were extremely rare in either group. The signal-averaged electrocardiographic parameters examined were also not significantly affected by the presence of mild LVH. Arrhythmia-related symptoms or malignant ventricular arrhythmia events were not observed in either group of patients during follow-up with antihypertensive treatment. The latter resulted in LVH regression in the 65 patients with mild LVH at baseline. It appears that mild LVH among ambulatory hypertensive patients does not carry an additive arrhythmogenic risk and can be successfully reversed with the appropriate antihypertensive therapy, with no need of additional antiarrhythmic management.     

Antithrombotic therapy after mitral valve repair: VKA or aspirin?

The optimal antithrombotic therapy following mitral valve repair (MVr) is still a matter of debate. Therefore, we evaluated the rate of thromboembolic and bleeding complications of two antithrombotic prevention strategies: vitamin K antagonists (VKA) versus aspirin. Consecutive patients who underwent MVr between 2004 and 2016 at three Dutch hospitals were evaluated for thromboembolic and bleeding complications during three postoperative months. The primary endpoint was the combined incidence of thromboembolic and bleeding complications to determine the net clinical benefit of VKA strategy as compared with aspirin. Secondary objectives were to evaluate both thromboembolic and bleeding rates separately and to identify predictors for both complications. A total of 469 patients were analyzed, of whom 325 patients (69%) in the VKA group and 144 patients (31%) in the aspirin group. Three months postoperatively, the cumulative incidence of the combined end point of the study was 9.2% (95%CI 6.1–12) in the VKA group and 11% (95%CI 6.0–17) in the aspirin group [adjusted hazard ratio (HR) 1.6, 95%CI 0.83–3.1]. Moreover, no significant differences were observed in thromboembolic rates (adjusted HR 0.82, 95%CI 0.16–4.2) as well as in major bleeding rates (adjusted HR 1.89, 95%CI 0.90–3.9). VKA and aspirin therapy showed a similar event rate of 10% during 3 months after MVr in patients without prior history of AF. In both treatment groups thromboembolic event rate was low and major bleeding rates were comparable. Future prospective, randomized trials are warranted to corroborate our findings.     

Can insulin action induce myocardial texture alterations in essential hypertension?

The prevalence of hyperinsulinemia/insulin resistance in hypertensive individuals, as well as the effects of insulin on myocytic and fibroblastic growth, are well known in both epidemiologic and animal models. To check whether there are any links between ultrasonic myocardial texture parameters and insulin level in essential hypertensives, we compared 18 essential hypertensive men (Group 1, H) with 18 age- and gender-matched healthy controls (Group 2, C) (age, 57 +/- 10 years). For all study subjects we performed ambulatory blood pressure monitoring (ABPM); conventional 2-D Doppler echocardiography for the assessment of the left ventricular mass index (LVMi) and function; quantitative analysis of digitized echocardiographic images for evaluation of cyclic variation (CVI) of mean gray level (MGL) at the septum and posterior wall levels; and 75-g 3-h oral glucose tolerance test (OGTT) for analysis of area under glycemic curve (AUGC, g/min/dL) and insulinemic curve (AUIC, mU/min/mL), as well as serum glucose and insulin peaks. Both the daily mean blood pressure (H: 109 +/- 4.6 v C: 94.6 +/- 4.6, P < .0001) and LVMi (adjusted for body surface) (H: 133 +/- 24 v C: 97 +/- 21 g/m2, P < .0001) were significantly higher in hypertensives. Values for AUIC were significantly higher in hypertensives (10.37 +/- 5.53 v 6.33 +/- 5.28), P < .032); CVI was also significantly higher in group C, for both septum (C: 40.2 +/- 16.9 v H: 15.9 +/- 18.1, P < .0001) and posterior wall (C: 44.5 +/- 19.6 v H: 20 +/- 17.5; P < .0001). There was a significant inverse correlation between AUIC and CVI for both septum (r: -0.57, P < .001) and posterior wall (r: -0.50, P < .002). The significantly higher impairment of myocardial ultrasonic texture and the higher level of the AUIC insulinemia in hypertensives, as well as the significant inverse relationship between CVI and hyperinsulinemia, are our major findings. Hyperinsulinemia/insulin resistance could cause an altered collagen/muscular ratio, which could potentially explain, at least in part, the CVI alterations detected in hypertensive patients.     

Pentoxifylline therapy: a new adjunct in the treatment of pulmonary hypertension?

Patients with markedly elevated pulmonary vascular resistance, whether caused by primary pulmonary hypertension or by congenital heart disease, have a grave prognosis, regardless of the type of therapy they undergo. This brief report presents our experience in treating 6 patients (4 women and 2 men) having pulmonary vascular obstructive disease, by administrating pentoxifylline (Trental), a drug that has been used in patients with chronic occlusive systemic arterial disease. Our patients underwent treadmill testing before the study and again 1 to 3 months after initiation of the study. Duration of exercise was short in all patients; however, it increased significantly while patients were taking pentoxifylline. These preliminary results are encouraging; however, we were unable to confirm other physiologic improvement with noninvasive study, and placebo effect was not ruled out. Therefore, we believe that use of pentoxifylline in patients with pulmonary vascular obstructive disease warrants further investigation by means of detailed direct hemodynamic measurement.     

Arginine therapy: a new treatment for pulmonary hypertension in sickle cell disease?

Pulmonary hypertension is a life-threatening complication of sickle cell disease. L-Arginine is the nitrogen donor for synthesis of nitric oxide, a potent vasodilator that is deficient during times of sickle cell crisis. This deficiency may play a role in pulmonary hypertension. The enzyme arginase hydrolyzes arginine to ornithine and urea, and thus, it may compete with nitric oxide synthase, leading to decreased nitric oxide production. Nitric oxide therapy by inhalation has improved pulmonary hypertension associated with acute chest syndrome in sickle cell disease, and several studies demonstrate therapeutic benefits of arginine therapy for primary and secondary pulmonary hypertension. We sought to determine the effects of arginine therapy on pulmonary hypertension in patients with sickle cell disease. Arginase activity was also determined. Oral arginine produced a 15.2% mean reduction in estimated pulmonary artery systolic pressure (63.9 +/- 13 to 54.2 +/- 12 mm Hg, p = 0.002) after 5 days of therapy in 10 patients. Arginase activity was elevated almost twofold (p = 0.07) in patients with pulmonary hypertension and may limit arginine bioavailability. With limited treatment options and a high mortality rate for patients with sickle cell disease who develop pulmonary hypertension, arginine is a promising new therapy that warrants further investigation.     

Patterns of left ventricular hypertrophy in essential hypertension: should echocardiography guide the pharmacological treatment?

The experimental design of clinical studies, on the pharmacological treatment of essential hypertension, has ignored a fundamental issue: Hypertensive patients are not a homogenous population. The adaptation of the cardiovascular system to hypertension is structurally and functionally heterogeneous. Recent clinical investigations suggest that this heterogeneity can be minimized by echocardiography. Thus, when the hemodynamic and neurohormonal profiles of untreated hypertensive patients are considered, in the particular context of the cardiac morphologic adaptation to high blood pressure, distinct common denominators emerge. Concentric and eccentric hypertrophy, the two most common patterns of ventricular hypertrophy, are at the extremes of the geometric spectrum. Concentric hypertrophy is characterized by an elliptic left ventricle, normal stroke volume and high peripheral vascular resistance. Its predominant neurohormonal profile includes elevated plasma renin and natriuretic peptide levels. Conversely, most patients with eccentric hypertrophy have a spheric left ventricle, increased stroke volume and low peripheral vascular resistance. Its corresponding neurohormonal profile shows low serum renin and enhanced sympathetic nervous activity. The therapeutic response, to angiotensin II antagonists and to beta-adrenergic blockers, of these two geometric patterns is also different. Concentric hypertrophy is substantially reversed by losartan, whereas, eccentric hypertrophy is refractory to both, losartan and atenolol. These facts raise a relevant question: Should ventricular geometry be considered when deciding which antihypertensive drug is to be prescribed?     

Hydroxychloroquine and chloroquine in COVID-19: should they be used as standard therapy?

Clinical Rheumatology - The pandemic of the new coronavirus, known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has urged the nations to an unprecedented world-wide reaction,...     

Older adults: Should the paradigm shift from standard therapy?

For older adults (ie, those age 60 and above) with acute myelogenous leukemia, patient and clinician have three choices: standard therapy, ie, a "3+7" regimen or low-dose ara-C, investigational therapy, or palliative care. Investigational treatments sponsored by pharmaceutical companies tend to exclude the 10-20% of older patients who have a poor performance status (Zubrod >2), an increased bilirubin, or creatinine (>1.9 mg/ml) and who are thereby unlikely to do well with standard therapy. However, even excluding such patients, standard treatment offers little obvious benefit for most older patients. Nonetheless, these older patients are not uniform and can be stratified to receive investigational therapy, which is mandatory for most, or standard therapy, which is not inappropriate for some.     

Consolidation therapy: What should be the standard of care?

Adults 18-60 years old with acute myelogenous leukemia (AML) should undergo some form of postremission therapy, however, how much and what kinds of postremission chemotherapy remain unclear. In contrast, for older patients more than one cycle of chemotherapy postremission does not appear justified except perhaps in those rare patients with favorable cytogenetics who are young enough to tolerate standard therapy and in whom there is still an option for cure. Routine postremission therapy is not justifiable for those with unfavorable cytogenetics. However, the median age of AML patients approaches 70 years; this is a group of patients who often reach minimal disease, but with a median disease-free survival of only 4 to 5 months, regardless of their cytogenetics, and are therefore an ideal patient group for clinical studies. Older patients have limited tolerance for intensive regimens, although relatively nontoxic agents exist that can be explored. The issue of maintenance remains open.