ABSTRACT

Treatment-resistant hypertension (TRH) is defined as office blood pressure (BP) uncontrolled on ≤3 or controlled on ≥4 antihypertensive medications at optimal doses. Apparent (a) TRH, a term used when medication dose, patient adherence, and out-of-office BP are unknown, impacts ~30% of treated, uncontrolled hypertensives. Approximately 50% of uncontrolled aTRH patients were not prescribed optimal therapy defined as ≥50% of maximum recommended doses of three different BP medication classes. Suboptimal adherence occurs in ~10 to 60% of aTRH cases. Out-of-office readings are nonhypertensive in roughly one-third of aTRH patients. Only ~30 to <50% of aTRH patients are truly treatment resistant. “Office” TRH has a favorable prognosis, underlining the importance of out-of-office BP. Suboptimal regimens and adherence with hypertension outside the office are likely associated with poor outcomes. Standardized treatment algorithms can improve appropriate prescribing. The BP self-monitoring, single-pill combinations, inexpensive medications, and shared decision making can improve adherence. Controlled TRH does not produce the expected reduction of cardiovascular events, suggesting that greater attention to other vascular risk factors and subclinical target organ change is important. The TRH patients have secondary hypertension more often than non-TRH patients, especially primary aldosteronism, yet most will not have an identifiable secondary cause. Many TRH patients are volume expanded and respond to intensified diuretic therapy, dietary sodium restriction, dual calcium channel blocker therapy, or addition of ƒ¿1-adrenoceptor antagonists. Plasma renin activity or hemodynamics can also inform successful and more personalized therapy. Referral to a hypertension specialist can be helpful if the approaches noted do not control BP in TRH.

Keywords: Cardiovascular disease, Nonadherence, Office resistance, Pseudoresistant hypertension, Spironolactone, Treatment-resistant hypertension.

How to cite this article: Egan BM. Treatment-Resistant Hypertension: A Pragmatic Management Approach. Hypertens J 2017;3(3):125-130.

Source of support: Nil

Conflict of interest: None

ABSTRACT

The cardiovascular continuum has been recognized for the past three decades in which antecedent risk factors, including hypertension and obesity, contribute to structural and functional cardiac and vascular changes. These risk factors and pathophysiological changes lead to left ventricular hypertrophy, myocardial infarction, cardiac dysfunction, heart failure, and death. Sudden death occurs more often among individuals with left ventricular hypertrophy, myocardial infarction, and heart failure. Several lines of evidence establish links between the sympathetic nervous system (SNS), heart rate, and cardiovascular risk factors, such as hypertension, inflammation, insulin resistance, and diabetes. These antecedent factors, with ongoing contributions from increased sympathetic drive and faster heart rates, often progress to asymptomatic functional and structural cardiovascular disease and subsequently to clinical cardiovascular disease and death, including sudden death. Increased sympathetic drive and faster heart rates can reflect familial and presumably genetic factors, various acute and chronic stressors, and obesity, especially abdominal-visceral obesity, which alter sympathovagal balance. Interventions, including lifestyle changes and pharmacotherapy that reduce heart rate and sympathetic drive, can interrupt the cardiovascular continuum at several points in this progressively deleterious pathway. Given the global obesity epidemic and the stresses of contemporary life, which can include crime, noise, and less stable families, it is important for clinicians to understand the role of increased sympathetic drive and faster heart rates in the continuum of cardiovascular risk, clinical cardiovascular disease, and death. Clinicians should be prepared to offer their patients lifestyle guidance and pharmacotherapy to interrupt this continuum and enhance cardiovascular health.

Keywords: Cardiovascular disease, Nonadherence, Office resistance, Pseudoresistant hypertension, Spironolactone, Treatment-resistant hypertension.

How to cite this article: Egan BM. Increased Sympathetic Drive, Elevated Heart Rate, and the Cardiovascular Continuum. Hypertens J 2017;3(3):105-112.

Source of support: Nil

Conflict of interest: None

ABSTRACT

Management of hypertension in pregnancy is a challenge, since the spectrum spreads from asymptomatic status to life-threatening complications like eclampsia. The time-tested American College of Obstetricians and Gynecologists (ACOG) classification fails to precisely prognosticate outcome of this complicated spectrum. Detection and risk stratification has undergone significant conceptual changes with the newer understanding of pathophysiology of this complex problem, mandating change in diagnostic algorithms. Introduction of biochemical high-risk markers like soluble fms-like tyrosine kinase 1 (sFlt-1):placental growth factor (PlGF) ratio has profoundly impacted risk stratification. A new four-question-based algorithm is suggested and its implications are discussed.

Keywords: Algorithm, Eclampsia, Hypertension, Preeclampsia, Pregnancy.

How to cite this article: Nair T, Nair A. Hypertension in Pregnancy: Do We need a New Algorithm? Hypertens J 2017;3(3):113-117.

Source of support: Nil

Conflict of interest: None

ABSTRACT

Congestive heart failure is a serious condition with high prevalence of morbidity and premature mortality. If not properly treated, congestive heart failure (CHF) has the same adverse prognosis as a malignancy. It is important to identify CHF early so that its progression to end-stage heart disease can be avoided. In addition to clinical suspicion, certain biomarkers can be utilized in the diagnosis and management of CHF. Thus, appropriate management of CHF with require clinical diagnosis combined with rational utilization of biomarkers. Recent advances in biochemical technology have confirmed the usefulness of certain biomarkers in the detection diagnosis and treatment of CHF.

Keywords: Biomarkers, Clinical diagnosis, Heart failure, Morbidity, Prognosis.

How to cite this article: Banerjee AK. Biomarkers in Congestive Heart Failure: Clinical Importance. Hypertens J 2017; 3(3):118-124.

Source of support: Nil

Conflict of interest: None

ABSTRACT

Primary aldosteronism (PA) was described over 60 years ago, but the relevance of PA to the burden of hypertension has never been greater. Best estimates from studies in a variety of settings indicate that PA is present in 5 to 8% of all patients with hypertension and up to 20% of patients with resistant hypertension. Progress in our understanding of the pathogenesis of PA helps to explain how PA can be so common and the genesis of bilateral hyperaldosteronism (BHA). Pitfalls in the evaluation of PA certainly exist, but these difficulties with the later stages of the evaluation should not impede liberal screening in groups of patients with a high prevalence of PA. In fact, the initial stages of the evaluation are utterly simple, and screening can make an enormous impact on the care of these patients. This article will provide a practical review of the approach to the patient suspected of having PA, which is by far the most common cause of secondary hypertension.

Keywords: Adrenal adenoma, Adrenal hyperplasia, Aldosterone, Hypertension, Hypokalemia, Ion channel, Primary aldosteronism, Renin.

How to cite this article: Auchus RJ. Clinical and Laboratory Assessment of Patients with Suspected Primary Aldosteronism. Hypertens J 2017;3(3):131-138.

Source of support: Nil

Conflict of interest: None

ABSTRACT

Left ventricular Hypertrophy (LVH) is an important consequence of systemic hypertension and is considered as target organ damage. LVH has significant impact on the prognosis and regression of LVH correlates with better outcomes in hypertensive individuals. Electrocardiography (ECG) remains the basic tool to diagnose LVH in hypertension although it has significant limitations in terms of sensitivity and specificity. Echocardiography not only provides a better estimate of LVH but also allows better quantification of left ventricular mass and volumes, while providing clues for other causes of LVH. Cardiac magnetic resonance Imaging (CMR) is considered the gold standard for estimation and characterization of LVH, but is limited due to its availability and cost. Computed Tomography of heart also offers reliable estimate of LVH at the cost of high radiation exposure and is not recommended for this purpose. Assessment of LVH should be done using ECG in every patient with hypertension while echocardiography and CMR should be reserved for specific indications

Keywords: Electrocardiography, Hypertension, Left ventricular hypertrophy.

How to cite this article: Deshpande MV, Deshpande NV. Assessment of End Organ Damage in Hypertension—Left Ventricular Hypertrophy. Hypertens J 2017;3(3):139-146.

Source of support: Nil

Conflict of interest: None

ABSTRACT

Dyslipidemia contributes to 50% of atherogenic cardiovascular events (CVEs). Statins decrease low-density lipoprotein cholesterol (LDL-C) on an average of 1 mmol and this is transformed into 20 to 25% reduction in CVE. Proprotein convertase subtilisin/kexin type 9 (PCSK9) fully humanized monoclonal antibodies (MoAbs) decrease LDL-C by another 1 to 1½ mmol on top of statins and this decreases CVE by another 20%. Therefore, the era has come when we are able to minimize the dyslipidemia-related atherogenic risk to a very great extent. The PCSK9 MoAbs require 12 to 26 injections per year. Inclisiran, which is a small interfering ribonucleic acid (siRNA), has shown to decrease LDL-C consistently for 6 months after a single injection. It is therefore emerging as a very important competitor to PCSK9 MoAbs. The future ongoing trials will tell us more about this molecule.

Keywords: Alirocumab, Proprotein convertase subtilisin/kexin type 9 inhibitors evolocumab, Small interfering ribonucleic acid.

How to cite this article: Manoria PC, Mishra N. Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors: Ready to Target Atherosclerotic Cardiovascular Disease beyond Statins. Hypertens J 2017;3(3):147-153.

Source of support: Nil

Conflict of interest: None

ABSTRACT

Diabetic nephropathy (DN) is the most common cause of end-stage renal disease worldwide. Sodium-glucose-linked transporter 2 (SGLT2) inhibitors are a new and promising class of antidiabetic agents that target renal tubular glucose reabsorption. Their action is based on the blockage of SGLT2 sodium- glucose cotransporters that are located at the luminal membrane of tubular cells of the proximal convoluted tubule (PCT), inducing glucosuria. It has been proven that they significantly reduce glycated hemoglobin (HbA1c), along with fasting and postprandial plasma glucose in patients with type II diabetes mellitus (T2DM). Glomerular hyperfiltration is a potential risk factor for DN. The SGLT2 inhibitors reduce sodium reabsorption in the proximal tubule, causing, through tubuloglomerular feedback (TGF), afferent arteriole vasoconstriction and reduction in hyperfiltration. The SGLT2 inhibitors reduced glomerular hyperfiltration in patients with T1DM, and in patients with T2DM, they caused transient acute reductions in glomerular filtration rate (GFR), followed by a progressive recovery and stabilization of renal function. Interestingly, recent studies consistently demonstrated a reduction in albuminuria. Recently, it was demonstrated that empagliflozin presents a significant cardioprotective effect. Although the SGLT2 inhibitors’ efficacy is affected by renal function, new data have been presented that some SGLT2 inhibitors, even in mild and moderate renal impairments, induce significant HbA1c reduction. Although these data are promising, only dedicated renal outcome trials will clarify whether SGLT2 inhibitors, in addition to their glycemic and blood pressure (BP) benefits, may provide nephroprotective effects.

Keywords: Diabetic kidney disease, Hyperfiltration, Renoprotection, Sodium-glucose-linked transporter 2 inhibitors.

How to cite this article: Chakravarthi MR, Marri HK. Renal Effects of Sodium-glucose-linked Transporter 2 Inhibitors. Hypertens J 2017;3(3):154-160.

Source of support: Nil

Conflict of interest: None

ABSTRACT

Diabetes mellitus is a major health problem in our country, and the prevalence is on the increase. Cardiovascular complications are the commonest causes of mortality and morbidity in patients with type II diabetes mellitus. Diabetes may not be a coronary artery disease (CAD) equivalent, but it certainly carries a high risk for atherosclerotic cardiovascular disease (CVD). There are effective drugs to treat hyperglycemia, and these drugs may be having adverse effects or advantageous outcomes on CVD, or they may be neutral. While developing antidiabetic drugs, it has become necessary to study their effect on CVD and outcome.

Among the newer antidiabetic drugs, sodium glucose cotransporter 2 (SGLT2) inhibitors have exhibited impressive cardiovascular benefits. Various mechanisms have been proposed to explain their improved cardiovascular outcome. They are not without adverse effects. There are a number of SGLT2 inhibitor preparations, and it is debatable whether this cardiovascular benefit is a class effect or individual drug specific. These newer antidiabetic drugs are looking beyond blood sugar control.

Keywords: Cardioprotective antidiabetic drugs, Heart and diabetes, Sodium glucose cotransporter 2 inhibitors.

How to cite this article: Iyengar SS. Cardiovascular Protective Actions of Sodium Glucose Cotransporter 2 Inhibitors. Hypertens J 2017;3(3):161-165.

Source of support: Nil

Conflict of interest: None