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Hypertension
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Malignant hypertension damages target organs and can cause a variety of complications. These include hypertensive encephalopathy, acute left ventricular failure with pulmonary edema, preeclampsia and eclampsia, acute aortic dissection, myocardial ischemia, and renal failure. The damage progresses quickly and is often fatal. Hypertensive encephalopathy may develop from a failure of the blood flow being autoregulated by the cerebrum. With this condition, there are usually manifestations such as cotton-wool spots, sclerosis, arteriolar narrowing, hemorrhage, and papilledema. Some amount of retinopathy is present in many other types of hypertensive emergencies. Cerebral deficits such as confusion, obtundation, or coma – regardless of the presence of focal deficits – are suggestive of encephalopathy. If there is a normal mental status with focal deficits, this suggests a stroke. Pulmonary edema is suggested by basilar lung crackles, jugular venous distention, and a third heart sound. Aortic dissection is suggested by asymmetry of pulses between the arms.
Non-DR Retinal Vascular Diseases
Published in Ching-Yu Cheng, Tien Yin Wong, Ophthalmic Epidemiology, 2022
Sobha Sivaprasad, Luke Nicholson, Shruti Chandra
Apart from chronic hypertensive retinopathy changes, sudden elevation of arterial pressure can lead to a rare clinical syndrome called malignant hypertension. It presents with rapid and severe elevation of blood pressure with the systolic component above 200 mmHg or the diastolic reading greater than 140 mmHg. Apart from absolute blood pressure recordings, systemic features that define malignant hypertension include ocular, cardiac, renal, and cerebral injury. If left untreated, persistently elevated malignant hypertension can lead to a rapidly fatal course due to end-organ failure, e.g., myocardial infarction, stroke, renal or cardiac failure (46). Malignant hypertension is seen in nearly 1% of hypertensive patients and is rarely the presenting symptom for hypertension. Well-controlled hypertensive patients seldom manifest with malignant hypertension, and survival rates with effective antihypertensive treatment are nearly 50% for more than 5 years (64). The average age at diagnosis for malignant hypertension is 40 years and most patients have pre-existing primary or secondary hypertension at presentation.
The cardiovascular system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Mary N Sheppard, C. Simon Herrington
Patients with malignant hypertension are ill. If they survive the usual complications of raised blood pressure – heart failure and cerebral haemorrhage – renal failure becomes universal and is the most common cause of death in untreated cases. Occasionally ‘hypertensive encephalopathy’ occurs, a syndrome characterized by altered consciousness, fits, and transient paralyses. The renal damage and encephalopathy are due to failure of autoregulation when the resistance vessels cease to protect the microcirculation from the increased pressure. This is rare in elderly people because the cerebral autoregulatory curve is shifted to the right (see Figure 7.17), but is more common in young people and especially in children whose arteries are unprotected by arteriosclerosis. Malignant hypertension causes: Renal failureHeart failureStrokeHypertensive encephalopathyMicroangiopathic haemolytic anaemia
Hyperhomocysteinemia: a trigger for complement-mediated TMA?
Published in Acta Clinica Belgica, 2021
J Bernards, P Doubel, G Meeus, E Lerut, A Corveleyn, L P Van Den Heuvel, W Meersseman, D K Kuypers, KJ Claes
To our knowledge, this is the first report of a patient with isolated hyperhomocysteinemia due to documented MTHFR deficiency and biopsy-proven TMA. The potential contribution of the isolated elevation in homocysteine on the one hand and the possibly pathogenic mutations in the genes encoding CFH and CFB on the other hand remains elusive. We hypothesize that the marked elevation in homocysteine might have led to endothelial dysfunction triggering the uncontrolled activation of a defective alternative complement pathway. However, the differential diagnosis with malignant hypertension remains, despite the absence of hypertension in the history of this patient. Circumstantial evidence does give some indication of the possible vasculopathic influence of the MTHFR polymorphism. Hyperhomocysteinemia caused by the MTHFR polymorphism has been linked to hypertension induced by vasoconstriction, renal dysfunction and sodium reabsorption [12–14]. MTHFR deficiency as a cause of hypertension has been studied in different populations with conflicting results [15–17]. In patients with idiopathic vascular lesions on kidney biopsy, prothrombotic mutations such as the MTHFR polymorphism showed to be more prevalent than in a control population [18]. Besides vascular edema and presence of thrombi intima fibrosis was found in the kidney biopsy of our patient .
Acute blood pressure elevation associated with biological therapies for cancer: a focus on VEGF signaling pathway inhibitors
Published in Expert Opinion on Biological Therapy, 2019
Giacomo Pucci, Alberto Milan, Anna Paini, Massimo Salvetti, Alberto Cerasari, Gaetano Vaudo
Malignant hypertension is a rare condition, usually described as the coexistence of very high BP levels, acute renal failure, advanced retinopathy (such as retinal hemorrhages, cotton wool spots or papilledema) and/or thrombotic microangiopathy. Given the systemic nature of this condition, the name of the syndrome has been recently proposed to be changed in ‘acute hypertensive microangiopathy’ [1]. The acute phase of the disease is induced by the concomitant occurrence of endothelial dysfunction, pressure natriuresis and volume depletion which, in turn, result in ischemia of the renovascular microcirculation, acute renal failure, and activation of the renin-angiotensin-aldosterone (RAA) system. The subsequent BP increase induced by disproportionate RAA activation, with levels of plasma renin activity more than three times higher than normal, determines the basis of a vicious cycle. Manifestations of thrombotic microangiopathy, such as fibrinoid necrosis, hemolytic anemia, decreased platelet count, increased lactate dehydrogenase (LDH) serum levels and presence of schistocytes, have often been described during the acute phase of malignant hypertension and highly correlate with the activation of the RAA system [46].
Pharmacological management of malignant hypertension
Published in Expert Opinion on Pharmacotherapy, 2020
Joanna Lewek, Agata Bielecka-Dąbrowa, Marek Maciejewski, Maciej Banach
Hypertension serves as a risk factor for cardiovascular diseases. One of its severe forms is malignant hypertension. Current European Society of Cardiology (ESC) and the European Society of Hypertension (ESH) guidelines [1] enlist malignant hypertension (MHT) as an urgency and emergency emphasizing that it is severe (most often grade 3 hypertension) and has poor prognosis if untreated [2–5]. Over the last decades, there have been many controversies over the definition of MHT. The traditional understanding of the term ‘malignant hypertension’ means that hypertension is severe and is accompanied by funduscopic changes including retinal flame hemorrhages, exudates, spots sometimes with papilledema. The first objection to that definition is that it does not offer exact values of blood pressure (BP) from which MHT should be diagnosed. Amongst some of the values present in different papers, there is 150 mmHg of mean arterial pressure [6] and 130 mmHg of diastolic BP [7]. Another objection is that the definition includes only one target organ damage, which probably corresponds to the fact that when it was created there were no other techniques for assessment of other organ damage. Nowadays, it seems that it should be expanded because other organ damage can be easily diagnosed [8,9]. Moreover, ischemic lesions may appear earlier in other organs, so diagnosis should not be delayed. The controversies over MHT definition has resulted in new proposals to requalify it to hypertension-MOD (multi organ damage) [3,10].The ESC/ESH guidelines now present an expanded definition which includes other ischemic target organ damage (funduscopic changes including papilledema or flame hemorrhages, microangiopathy, disseminated intravascular coagulation, encephalopathy, acute heart failure and acute deterioration in renal function) [1]. The guidelines devote a particularly small amount of space to MHT. Even that reflects that the topic of malignant hypertension is not fully understood and that it needs further studies which is rather difficult taking into account it’s prevalence and the need for rapid management.