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Dr. Renata Cifkova ,
C Tsioufis (Athens, Greece) covered the topic of perioperative management of hypertension. Preoperative patient evaluation is an opportunity to check and optimize control of hypertension. The extent of diagnostic approach beyond history, physical examination, laboratory evaluation, and ECG depends on the urgency of surgery and the surgery-specific risk, the presence of active cardiac condition and other risk factors and the functional capacity of the patient. Patients with well-controlled hypertension are less likely to experience intraoperative BP instability and postoperative complications than patients with poorly controlled hypertension. Ideally, BP should be normalized for several months prior to elective surgery. In patients with grade I-II hypertension, there is no evidence that delay in surgery in order to optimize therapy is beneficial. In patients with grade III hypertension (BP 180/110 mmHg), the potential benefits of delayed surgery to optimize the pharmacological treatment should be weighed against the risk of delaying the surgical procedure. In the case of urgent surgery, the patient should be treated with a parenteral drug acutely. Patients on chronic antihypertensive treatment should continue taking their medications until the time of surgery.
A Coca (Barcelona, Spain) reviewed the topic of hypertension in acute stroke. Stroke is one of the major causes of mortality and disease burden in Europe and worldwide because of residual disability and cognitive decline. Thromboembolic occlusions of large arteries are the most common cause of stroke, and hypertension and age are the most important risk factors. For this reason, prevention of incident stroke and stroke recurrence is mostly based on BP-lowering therapy. While the value of BP reduction in decreasing incident stroke is well proven, no conclusive evidence is available on the optimal level to which BP should be reduced: the concept that the lower the BP achieved, the greater the outcome reduction has often been challenged by the hypothesis that a J-shaped relationship exists between BP achieved by treatment and incident cardiovascular events. Another controversial issue is the management of high BP in the acute phase of stroke. Elevations in SBP > 160 mmHg are detected in more than 60% of patients with acute stroke and are associated with poor outcome after stroke. Theoretical reasons for lowering BP include reducing the formation of brain edema, lessening the risk of hemorrhagic transformation of the infarction, preventing further vascular damage, and forestalling early recurrent stroke. On the other hand, aggressive treatment of high BP may lead to neurological worsening by reducing perfusion pressure to ischemic areas of the brain. The question whether BP should be lowered in all patients with acute ischemic stroke and high BP values is still unanswered despite the recent results of the SCAST study. Other studies designed to provide definite answers to these questions such as ENOS and INTERACT are still ongoing.
S Kjeldsen (Oslo, Norway) addressed the issue of hypertensive emergencies and urgencies. Hypertensive emergencies can be defined as severe elevations of BP in the presence of acute target organ damage (TOD). Acute coronary syndromes, dissecting aortic aneurysms, acute pulmonary edema, hypertensive encephalopathy (malignant hypertension), acute cerebral infarction, intracerebral hemorrhage, or acute arterial bleeding or eclampsia have represented clinical conditions in which an immediate BP reduction were considered necessary to prevent TOD progression. Exceptions now are acute stroke. Hypertensive urgencies are characterized by severe elevations in BP (180/120 mmHg) without evidence of acute TOD. In hypertensive urgencies, BP can usually be reduced in the emergency department by orally administered drugs without hospital admission and with ambulatory follow-up.
C Vlachopoulos (Athens, Greece) dealt with the topic of erectile dysfunction (ED), a very common problem in hypertensive patients. Approximately 1 out of 2 patients with hypertension have some degree of ED. The important question is whether ED is related to antihypertensive drug therapy or to hypertension itself. Undoubtedly, some antihypertensive drugs such as thiazide diuretics and beta-blockers cause ED through different mechanisms. Specifically for beta-blockers, their association with ED has been exaggerated and some, such as nebivolol, may even improve erectile function. ACE inhibitors and ARBs may also improve erectile function. Hypertension in itself may also lead to ED, so it is a common clinical mistake, either by doctors or by patients, to avoid medication fearing the side effect of ED. ED carries an independent risk for future cardiovascular events and a thorough cardiovascular investigation is advised in high-risk patients. Controlled hypertension itself does not preclude from further treatment for ED. Phosphodiesterase type 5 inhibitors (PDE5i), the commonest medication for ED, is effective in hypertensive patients, and these drugs can be safely co-administered with antihypertensive medication. Only alfa-blockers should be spaced a few hours apart with PDE5i intake, while the only absolute contraindication is co-administration of nitrates.
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