The pathophysiology of arterial hypertension is multifactorial. We could not consider all mechanisms (1). Unfortunately, the individual mechanisms that cause a rise in blood pressure usually cannot be identified. Our colleague Dr. Swalve-Bordeaux points out that blood pressure in postmenopausal women often increases and suggests that this increase in blood pressure should be counteracted with estrogen replacement. We consider this proposal to be extremely problematic, as recent meta-analyses of large clinical trials have shown that estrogen administration (with or without progesterone) in the context of primary prevention provides minor benefits in some areas, yet increases serious complications in others (2). For instance, receiving only estrogens increases the risk of stroke. In contrast, antihypertensive therapy has been clearly proven to reduce the risk of stroke. The comment that sleep deprivation is an underestimated risk factor for arterial hypertension is supported by epidemiological studies (3). We consider the decrease in mean sleep duration in many countries to be alarming. A form of secondary hypertension should be considered especially for patients with early onset hypertension, blood pressure that remains uncontrolled, or suspicious concomitant clinical symptoms and findings. Prof. Koch reminds us that these rarer diseases can have an atypical presentation. We should always subject clinical diagnoses—whether for hypertension or any other area of clinical medicine—to regular review. However, an untargeted search for cause in all patients with hypertension cannot be recommended.
We thank Dr. Regenthal for clarification of the adverse effects and drug interactions of calcium antagonists. The interaction between amlodipine and simvastatin is of importance because both drugs are prescribed very frequently. A combination of 80 mg simvastatin and 10 mg amlodipine per day has a potentially clinically relevant interaction. The maximum recommended dosage of simvastatin in concurrent use with amlodipine varies between 20 and 40 mg per day. If this dosage is insufficient, statins with a lower potential for interaction with amlodipine, such as atorvastatin, pravastatin, fluvastatin, or rosuvastatin, may be used.
Dr. Mehrländer questions the increasing emphasis on initial antihypertensive combination therapy using fixed combination preparations. In fact, there is no clear evidence that one or the other approach is preferable (4). As stated (1), we consider the initiation of combination therapy to be useful for patients with high blood pressure for whom a monotherapy is not expected to suffice for blood pressure control. For patients who are elderly or who present with concomitant diseases, having a greater control over the therapy by using free drug combinations may be beneficial.
Dr. Uebel and Dr. Egidi correctly stated that we did not take into account all the current guidelines. The S3 guideline on Risk Counseling on Cardiovascular Prevention in Family Medicine, in which Dr. Egidi was involved, provides a very meaningful framework for cardiovascular risk prevention. Not all clinical data included in the international hypertension guidelines have been included here. Most data on which the recommendations of current guidelines and our review are based have been generated in outpatient clinical trials. However, the patient population in clinical trials often represents a positive selection. The assertion that a guideline is only valid if it was created using the target group is unsubstantiated. The guidelines agree that lowering blood pressure can reduce cardiovascular risk, and especially the risk of stroke. However, lowering blood pressure too much also carries risks. Reviews and guidelines can only provide a framework for individual clinical decisions, especially when adjusting and implementing target values for blood pressure. Meaningful therapy decisions can only be made based on both clinical expertise and dialogue with the patient. Equally important is the good cooperation between primary care physicians, who care for the majority of patients with hypertension, and specialists, whose expertise is particularly required for difficult-to-adjust and complex cases.
On behalf of the authors:
Prof. Dr. med. Jens Jordan
Institut für Luft- und Raumfahrtmedizin,
Deutsches Zentrum für Luft- und Raumfahrt (DLR)
Conflict of interest statement
Prof. Jordan has received scientific consultant honoraria from Bayer, Eternygen, Johnson & Johnson, Novartis, Novo-Nordisk, and Theravance and is co-founder of Eternygen GmbH.
|1.||Jordan J, Kurschat C, Reuter H: Arterial hypertension—diagnosis and treatment. Dtsch Arztebl Int 2018; 115: 557–68 VOLLTEXT|
|2.||Gartlehner G, Patel SV, Feltner C, et al.: Hormone therapy for the primary prevention of chronic conditions in postmenopausal women: evidence report and systematic review for the US Preventive Services Task Force. JAMA 2017; 318: 2234–49 CrossRef MEDLINE|
|3.||Cappuccio FP, Stranges S, Kandala NB, et al.: Gender-specific associations of short sleep duration with prevalent and incident hypertension: the Whitehall II Study. Hypertension 2007; 50: 693–700 CrossRef MEDLINE PubMed Central|
|4.||Garjon J, Saiz LC, Azparren A, et al.: First-line combination therapy versus first-line monotherapy for primary hypertension. Cochrane Database Syst. Rev 2017; 1: Cd010316 CrossRef|