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Background: Thrombotic microangiopathy (TMA) is a complication of malignant hypertension (mHTN) attributed to high blood pressure (BP). However, no studies have investigated in patients with mHTN of different aetiologies whether the presence of TMA is associated with specific causes of mHTN., Methods: We investigated the presence of TMA (microangiopathic haemolytic anaemia and thrombocytopenia) in a large and well-characterized cohort of 199 patients with mHTN of different aetiologies [primary HTN 44%, glomerular diseases 16.6%, primary atypical haemolytic uraemic syndrome (aHUS) 13.1%, renovascular HTN 9.5%, drug-related HTN 7%, systemic diseases 5.5%, endocrine diseases 4.5%]. Outcomes of the study were kidney recovery and kidney failure., Results: Patients with TMA [40 cases (20.1%)] were younger, were more likely female and had lower BP levels and worse kidney function at presentation. Their underlying diseases were primary aHUS (60%), drug-related mHTN (15%), glomerular diseases [all of them immunoglobulin A nephropathy (IgAN); 10%], systemic diseases (10%) and primary HTN (5%). The presence of TMA was 92.3% in primary aHUS, 42.9% in drug-related HTN, 36.4% in systemic diseases, 12.1% in glomerular diseases and 2.3% in primary HTN. No patient with renovascular HTN or mHTN caused by endocrine diseases developed TMA, despite BP levels as high as patients with TMA. A higher proportion of TMA patients developed kidney failure as compared with patients without TMA (56.4% versus 38.9%, respectively)., Conclusions: The presence of TMA in patients with mHTN should guide the diagnosis towards primary aHUS, drug-related mHTN, some systemic diseases and IgAN, while it is exceptional in other causes of mHTN.

Malignant hypertension is listed among the causes of secondary thrombotic microangiopathy (TMA), but pathogenic mutations in complement genes have been reported in patients with hypertension-induced TMA. Here we investigated the frequency and severity of hypertension in 55 patients with primary atypical hemolytic uremic syndrome (aHUS). A genetic analysis was performed in all patients, and funduscopic examination was performed in all the patients with Grades 2 and 3 hypertension. A cohort of 110 patients with malignant hypertension caused by diseases other than aHUS served as control. Thirty-six patients with aHUS presented Grade 2 or Grade 3 hypertension and funduscopic examination showed malignant hypertension in 19. Genetic abnormalities in complement were found in 19 patients (37% among patients with malignant hypertension). Plasmapheresis was performed in 46 patients and 26 received eculizumab. Renal and hematological responses were significantly lower after plasmapheresis (24%) than after eculizumab (81%). Renal survival was significantly higher in patients treated with eculizumab (85% at one, three and five years) compared to patients who did not receive this treatment (54%, 46% and 41%), respectively. Response to eculizumab was independent of hypertension severity and the presence of complement genetic abnormalities. Among patients with malignant hypertension caused by other diseases the prevalence of TMA was very low (5%). Thus, severe and malignant hypertension are common among patients with aHUS and eculizumab treatment leads to a higher renal survival when compared to plasmapheresis. However, TMA is uncommon among patients presenting with malignant hypertension caused by diseases other than aHUS.

Thrombotic microangiopathy (TMA) arises in a variety of clinical circumstances with the potential to cause significant dysfunction of the kidneys, brain, gastrointestinal tract and heart. TMA should be considered in all patients with thrombocytopenia and anaemia, with an immediate request to the haematology laboratory to look for red cell fragments on a blood film. While TMA of any aetiology generally demands prompt treatment, this is especially so in thrombotic thrombocytopenic purpura (TTP) and atypical haemolytic uraemic syndrome (aHUS), where organ failure may be precipitous, irreversible and fatal. In all adults, urgent, empirical plasma exchange (PE) should be started within 4-8 h of presentation for a possible diagnosis of TTP, pending a result for ADAMTS13 activity (a disintegrin and metalloprotease thrombospondin, number 13). A sodium citrate plasma sample should be collected for ADAMTS13 testing prior to any plasma therapy. In children, Shiga toxin-associated haemolytic uraemic syndrome due to infection with Escherichia coli (STEC-HUS) is the commonest cause of TMA, and is managed supportively. If TTP and STEC-HUS have been excluded, a diagnosis of aHUS should be considered, for which treatment is with the monoclonal complement C5 inhibitor, eculizumab. While early confirmation of aHUS is often not possible, except in the minority of patients in whom autoantibodies against factor H are identified, genetic testing ultimately reveals a complement-related mutation in a significant proportion of aHUS cases. The presence of other TMA-associated conditions (e.g. infection, pregnancy/postpartum and malignant hypertension) does not exclude TTP or aHUS as the underlying cause of TMA.Copyright © 2018 Asian Pacific Society of Nephrology

Background Severe hypertension can induce thrombotic microangiopathy (TMA) in the renal vasculature, the occurrence of which has been linked to mechanical stress to the endothelium. Complement defects may be the culprit of disease in patients who present with severe renal disease and often progress to ESRD, despite BP control.Methods We studied a well defined cohort of 17 patients with hypertension-associated TMA to define the prevalence of complement defects by a specific ex vivo serum-based microvascular endothelial cell assay.Results Compared with normal human serum and samples from patients with hypertensive arterionephrosclerosis, 14 of 16 (87.5%) serum samples collected at presentation from 16 patients with hypertension-associated TMA induced abnormal C5b9 formation on microvascular endothelial cells. We detected rare variants in complement genes in eight of 17 (47%) patients. ESRD occurred in 14 of 17 (82%) patients, and recurrent TMA after transplant occurred in seven of 11 (64%) donor kidneys. Eculizumab improved the renal function in three patients and prevented TMA recurrence in an allograft recipient.Conclusions These observations point to complement defects as the key causative factor of ESRD and recurrent TMA after transplant in patients presenting with severe hypertension. Complement defects can be identified by measurements of complement activation on microvascular endothelial cells, which should substantially influence treatment and prognosis.

Thrombotic microangiopathy (TMA) arises in a variety of clinical circumstances with the potential to cause significant dysfunction of the kidneys, brain, gastrointestinal tract and heart. TMA should be considered in all patients with thrombocytopenia and anaemia, with an immediate request to the haematology laboratory to look for red cell fragments on a blood film. While TMA of any aetiology generally demands prompt treatment, this is especially so in thrombotic thrombocytopenic purpura (TTP) and atypical haemolytic uraemic syndrome (aHUS), where organ failure may be precipitous, irreversible and fatal. In all adults, urgent, empirical plasma exchange (PE) should be started within 4-8 h of presentation for a possible diagnosis of TTP, pending a result for ADAMTS13 activity (a disintegrin and metalloprotease thrombospondin, number 13). A sodium citrate plasma sample should be collected for ADAMTS13 testing prior to any plasma therapy. In children, Shiga toxin-associated haemolytic uraemic syndrome due to infection with Escherichia coli (STEC-HUS) is the commonest cause of TMA, and is managed supportively. If TTP and STEC-HUS have been excluded, a diagnosis of aHUS should be considered, for which treatment is with the monoclonal complement C5 inhibitor, eculizumab. While early confirmation of aHUS is often not possible, except in the minority of patients in whom autoantibodies against factor H are identified, genetic testing ultimately reveals a complement-related mutation in a significant proportion of aHUS cases. The presence of other TMA-associated conditions (e.g. infection, pregnancy/postpartum and malignant hypertension) does not exclude TTP or aHUS as the underlying cause of TMA.Copyright © 2018 Asian Pacific Society of Nephrology

Introduction Thrombotic microangiopathy (TMA) has been described with long-term interferon-beta (IFN-b). We report a case of biopsy-proven TMA in a patient with multiple sclerosis (MS) who had been having IFN-b-1a injections for twenty years. These biopsy findings were similar to previously described lung histological changes in IFN b- induced pulmonary arterial hypertension (PAH). Case A 57 year old woman with relapsing-remitting multiple sclerosis had been administering IFN-b-1a injections for twenty years. Her BMI was 21 and she was on a dose of 44 mcg three times per week. She presented with acute pulmonary oedema, renal failure, malignant hypertension, microangiopathic haemolytic anaemia and thrombocytopenia after one week of increasing dyspnoea. A renal biopsy showed malignant hypertensive nephropathy and microangiopathy consistent with TMA. Alternative TMA syndromes including haemolytic uraemic syndrome and thrombotic thrombocytopenic purpura were excluded. Renal function stabilised after the IFN was ceased but never returned to the baseline level. Results Her renal biopsy showed glomerular capillary thrombus deposition, endothelial reactivity, vessel necrosis and wall duplication with luminal thrombus. Fibromuscular proliferation, focal fibrinoid necrosis and luminal thrombus was also present within arterioles. These microvascular histopathological findings resemble vessel changes observed seen in lung biopsies in human IFN b mediated PAH, and those described in transgenic mouse models engineered to overproduce Type 1 IFN.1 2 Our patient was on treatment for twenty years at a dose exceeding 50 mcg per week. Both are postulated risk factors for the development of TMA.2 Conclusion Our report highlights similarities between microvascular changes seen in IFN-induced TMA and those observed in pulmonary arterial hypertension associated with IFN therapy. This suggests a shared pathophysiological mechanism. Kavanagh et al had described a dose-dependent spectrum of r

Background Severe hypertension can induce thrombotic microangiopathy (TMA) in the renal vasculature, the occurrence of which has been linked to mechanical stress to the endothelium. Complement defects may be the culprit of disease in patients who present with severe renal disease and often progress to ESRD, despite BP control.Methods We studied a well defined cohort of 17 patients with hypertension-associated TMA to define the prevalence of complement defects by a specific ex vivo serum-based microvascular endothelial cell assay.Results Compared with normal human serum and samples from patients with hypertensive arterionephrosclerosis, 14 of 16 (87.5%) serum samples collected at presentation from 16 patients with hypertension-associated TMA induced abnormal C5b9 formation on microvascular endothelial cells. We detected rare variants in complement genes in eight of 17 (47%) patients. ESRD occurred in 14 of 17 (82%) patients, and recurrent TMA after transplant occurred in seven of 11 (64%) donor kidneys. Eculizumab improved the renal function in three patients and prevented TMA recurrence in an allograft recipient.Conclusions These observations point to complement defects as the key causative factor of ESRD and recurrent TMA after transplant in patients presenting with severe hypertension. Complement defects can be identified by measurements of complement activation on microvascular endothelial cells, which should substantially influence treatment and prognosis.

Thrombotic microangiopathy (TMA) is a pattern of endothelial damage that can be found in association with diverse clinical conditions such as malignant hypertension. Although the pathophysiological mechanisms differ, accumulating evidence links complement dysregulation to various TMA syndromes and in particular the atypical hemolytic uremic syndrome. Here, we evaluated the role of complement in nine consecutive patients with biopsy-proven renal TMA attributed to severe hypertension. Profound hematologic symptoms of TMA were uncommon. In six Out of nine patients, we found mutations C3 in three, CFI in one, CD46 in one, and/or CFH in two patients either with or without the risk CFH-H3 haplotype in four patients. Elevated levels of the soluble C5b-9 and renal deposits of C3c and C5b-9 along the vasculature and/or glomerular capillary wall, confirmed complement activation in vivo. In contrast to patients without genetic defects, patients with complement defects invariably progressed to end-stage renal disease, and disease recurrence after kidney transplantation seems common. Thus, a subset of patients with hypertension-associated TMA falls within the spectrum of complement-mediated TMA, the prognosis of which is poor. Hence, testing for genetic complement abnormalities is warranted in patients with severe hypertension and TMA on renal biopsy to adopt suitable treatment options and prophylactic measures.

Thrombotic microangiopathy (TMA) is a pattern of endothelial damage that can be found in association with diverse clinical conditions such as malignant hypertension. Although the pathophysiological mechanisms differ, accumulating evidence links complement dysregulation to various TMA syndromes and in particular the atypical hemolytic uremic syndrome. Here, we evaluated the role of complement in nine consecutive patients with biopsy-proven renal TMA attributed to severe hypertension. Profound hematologic symptoms of TMA were uncommon. In six Out of nine patients, we found mutations C3 in three, CFI in one, CD46 in one, and/or CFH in two patients either with or without the risk CFH-H3 haplotype in four patients. Elevated levels of the soluble C5b-9 and renal deposits of C3c and C5b-9 along the vasculature and/or glomerular capillary wall, confirmed complement activation in vivo. In contrast to patients without genetic defects, patients with complement defects invariably progressed to end-stage renal disease, and disease recurrence after kidney transplantation seems common. Thus, a subset of patients with hypertension-associated TMA falls within the spectrum of complement-mediated TMA, the prognosis of which is poor. Hence, testing for genetic complement abnormalities is warranted in patients with severe hypertension and TMA on renal biopsy to adopt suitable treatment options and prophylactic measures.

Malignant hypertension is a severe form of hypertension which pathogenesis is not fully elucidated. The aim of our study was to investigate the role of Angiotensin II on hemodynamic and oxidative stress parameters in model of malignant hypertension by using losartan. Adult males were divided into three groups: normotensive Wister rats, control SHR and losartan treated SHR. Control and SHR group received a single bolus dosage of saline, while the SHR + LOS group received a losartan. Blood pressure, cardiac output, both total peripheral and carotid vascular resistance and carotid blood flow were measured. CAT, SOD and TBARS were determined in the blood samples. The treatment significantly decreased the blood pressure. There was no significant change in cardiac output or carotid blood flow, but treatment resulted in diminishment of vascular resistances, both total peripheral and carotid. There was a tendency to restore the values of SOD activity towards those of the normotensive group, but there were no change in CAT and TBARS levels. Taken together, our results show that a single application of losartan has a strong hypotensive effect. Angiotensin II seems to have a significant role in the malignant hypertension syndrome and it partially affects oxidative stress parameters., Maligna hipertenzija predstavlja posebno težak oblik hipertenzije čija patogeneza nije u potpunosti razjašnjena. Cilj naše studije bio je ispitivanje uloge Angiotenzina II (Ang II) u regulaciji hemodinamskih i parametara oksidativnog stresa u modelu maligne hipertenzije. Mužjaci odraslih pacova su podeljeni u tri grupe: normotenzivne Wistar pacove, kontrolne hipertenzivne (SHR) i losartanom tretirane hipertenzivne pacove (SHR+LOS). Kontrolna i SHR grupa su primile po jednu bolus dozu fiziološkog rastvora, dok je SHR+LOS grupa primila losartan, receptorni blokator Ang II, Nakon toga su mereni krvni pritisak, minutni volumen srca (MV), karotidni protok krvi (KPK) i određivani odgovarajući otpori: ukupni periferni otpor (UPO) i karotidni vaskularni otpor (KVO). Parametri oksidativnog stresa: aktivnost katalaze (CAT), aktivnost superoksid dismutaze (SOD) i marker lipidne peroksidacije (TBARS) su određivani iz uzoraka krvi. Tretman losartanom je značajno snizio vrednost krvnog pritiska. Nije došlo do značajnih promena vrednosti MV ni KPK, ali je tretman losartanom doveo do smanjenja UPO i KVO. U ovoj grupi je uočena tendencija povećanja aktivnosti SOD ka vrednostima normotenzivnih životinja, ali nije bilo promena u vrednostima CAT i TBARS. Naši rezultati pokazuju da jednokratna aplikacija losartana ima snažan hipotenzivni efekat i da Ang II igra značajnu ulogu u mehanizmima maligne hipertenzije, delimično preko antioksidativnog delovanja. PR Projekat Ministarstva nauke Republike Srbije, br. OI 175096.

Malignant hypertension is a severe form of hypertension which pathogenesis is not fully elucidated. The aim of our study was to investigate the role of Angiotensin II on hemodynamic and oxidative stress parameters in model of malignant hypertension by using losartan. Adult males were divided into three groups: normotensive Wister rats, control SHR and losartan treated SHR. Control and SHR group received a single bolus dosage of saline, while the SHR + LOS group received a losartan. Blood pressure, cardiac output, both total peripheral and carotid vascular resistance and carotid blood flow were measured. CAT, SOD and TBARS were determined in the blood samples. The treatment significantly decreased the blood pressure. There was no significant change in cardiac output or carotid blood flow, but treatment resulted in diminishment of vascular resistances, both total peripheral and carotid. There was a tendency to restore the values of SOD activity towards those of the normotensive group, but there were no change in CAT and TBARS levels. Taken together, our results show that a single application of losartan has a strong hypotensive effect. Angiotensin II seems to have a significant role in the malignant hypertension syndrome and it partially affects oxidative stress parameters., Maligna hipertenzija predstavlja posebno težak oblik hipertenzije čija patogeneza nije u potpunosti razjašnjena. Cilj naše studije bio je ispitivanje uloge Angiotenzina II (Ang II) u regulaciji hemodinamskih i parametara oksidativnog stresa u modelu maligne hipertenzije. Mužjaci odraslih pacova su podeljeni u tri grupe: normotenzivne Wistar pacove, kontrolne hipertenzivne (SHR) i losartanom tretirane hipertenzivne pacove (SHR+LOS). Kontrolna i SHR grupa su primile po jednu bolus dozu fiziološkog rastvora, dok je SHR+LOS grupa primila losartan, receptorni blokator Ang II, Nakon toga su mereni krvni pritisak, minutni volumen srca (MV), karotidni protok krvi (KPK) i određivani odgovarajući otpori: ukupni periferni otpor (UPO) i karotidni vaskularni otpor (KVO). Parametri oksidativnog stresa: aktivnost katalaze (CAT), aktivnost superoksid dismutaze (SOD) i marker lipidne peroksidacije (TBARS) su određivani iz uzoraka krvi. Tretman losartanom je značajno snizio vrednost krvnog pritiska. Nije došlo do značajnih promena vrednosti MV ni KPK, ali je tretman losartanom doveo do smanjenja UPO i KVO. U ovoj grupi je uočena tendencija povećanja aktivnosti SOD ka vrednostima normotenzivnih životinja, ali nije bilo promena u vrednostima CAT i TBARS. Naši rezultati pokazuju da jednokratna aplikacija losartana ima snažan hipotenzivni efekat i da Ang II igra značajnu ulogu u mehanizmima maligne hipertenzije, delimično preko antioksidativnog delovanja. PR Projekat Ministarstva nauke Republike Srbije, br. OI 175096.

Introduction: Malignant hypertension is high blood pressure that comes suddenly and quickly. We attempted to review the clinical and fundus findings in patients with malignant hypertension (MHT). The lower (diastolic) blood pressure reading which is normally less than 80 mmHg, is often above 130 mmHg (240/140mmHg). Malignant hypertension may present with retinopathy, choroidopathy, and optic neuropathy. Optical coherence tomography is a relatively new imaging technique for evaluating retinal thickness and the location of pathology in patients with malignant hypertension. Material and Methods: A retrospective observational study was carried in the department of ophthalmology comprising two groups based on history of history of hypertension (group1)and no history of hypertension (group2). The charts and fundus photographs of patients with hypertensive retinopathy from 2010 to 2015 was studied. Data of patients were included when their color photographs of the fundus were judged to indicate hypertensive retinopathy grade III or IV. There had to have been at least 1 high blood pressure reading recorded in the chart during the period when the symptoms occurred. Results: Twenty patients were included in our study. Patients were divided into 2 groups according to whether or not they had a history ofhypertension. Group 1 included 8 patients with no hypertension history, while group 2 included 12 patients with a known hypertension history. In group 1, Malignant hypertension was diagnosed by an ophthalmologist in 8 patients, in which 4:4 M:F ratio and In group 2 , 12 patients of malignant hypertension, in which M:F ratio being 3:9.There were no significant differences in age, or systolic and diastolic blood pressures. There were more complications such as renal failure and stroke in group 2 patients. Conclusion: Funduscopy has decisive significance in the diagnosis and monitoring of MHT. In order to accurately diagnose and achieve early control of this critical condition, a d

Introduction: Malignant hypertension is high blood pressure that comes suddenly and quickly. We attempted to review the clinical and fundus findings in patients with malignant hypertension (MHT). The lower (diastolic) blood pressure reading which is normally less than 80 mmHg, is often above 130 mmHg (240/140mmHg). Malignant hypertension may present with retinopathy, choroidopathy, and optic neuropathy. Optical coherence tomography is a relatively new imaging technique for evaluating retinal thickness and the location of pathology in patients with malignant hypertension. Material and Methods: A retrospective observational study was carried in the department of ophthalmology comprising two groups based on history of history of hypertension (group1)and no history of hypertension (group2). The charts and fundus photographs of patients with hypertensive retinopathy from 2010 to 2015 was studied. Data of patients were included when their color photographs of the fundus were judged to indicate hypertensive retinopathy grade III or IV. There had to have been at least 1 high blood pressure reading recorded in the chart during the period when the symptoms occurred. Results: Twenty patients were included in our study. Patients were divided into 2 groups according to whether or not they had a history ofhypertension. Group 1 included 8 patients with no hypertension history, while group 2 included 12 patients with a known hypertension history. In group 1, Malignant hypertension was diagnosed by an ophthalmologist in 8 patients, in which 4:4 M:F ratio and In group 2 , 12 patients of malignant hypertension, in which M:F ratio being 3:9.There were no significant differences in age, or systolic and diastolic blood pressures. There were more complications such as renal failure and stroke in group 2 patients. Conclusion: Funduscopy has decisive significance in the diagnosis and monitoring of MHT. In order to accurately diagnose and achieve early control of this critical condition, a d

Introduction: Hypertensive retinopathy describes a spectrum of retinal changes in patients with elevated blood pressure (BP). It is unknown why some patients are more likely to develop acute ocular end-organ damage than others with similar BP. We examined risk factors for grade III/IV hypertensive retinopathy among patients with hypertensive urgency in the emergency department (ED) and compared healthcare utilization and mortality between patients with and without grade III/IVhypertensive retinopathy.Methods: A preplanned subanalysis of patients who presented to a university hospital ED with diastolic BP 120 mmHg and who enrolled in the Fundus Photography versus Ophthalmoscopy Trial Outcomes in the ED study was performed. Bilateral nonmydriatic ocular fundus photographs, vital signs, and demographics were obtained at presentation. Past medical history, laboratory values, healthcare utilization, and mortality were ascertained from medical record review at least 8 months after initial ED visit.Results: Twenty-one patients with diastolic BP 120 mmHg, 7 of whom (33%) had grade III/IV hypertensive retinopathy, were included. Patients with retinopathy were significantly younger than those without (median 33 vs 50 years, P ¼ 0.02). Mean arterial pressure (165 vs 163 mmHg) was essentially equal in the 2 groups. Patients with retinopathy had substantially increased but nonsignificant rates of ED revisit (57% vs 29%, P ¼ 0.35) and hospital admission after ED discharge (43% vs 14%, P ¼ 0.28). One of the patients with retinopathy died, but none without.Conclusion: Younger patients may be at higher risk for grade III/IV hypertensive retinopathy among patients with hypertensive urgency. Chronic compensatory mechanisms may have not yet developedin these younger patients. Alternatively, older patients with retinopathy may be underrepresented secondary to increased mortality among these patients at a younger age (survivorship bias). Further research is needed to validate these preli

Introduction: Hypertensive retinopathy describes a spectrum of retinal changes in patients with elevated blood pressure (BP). It is unknown why some patients are more likely to develop acute ocular end-organ damage than others with similar BP. We examined risk factors for grade III/IV hypertensive retinopathy among patients with hypertensive urgency in the emergency department (ED) and compared healthcare utilization and mortality between patients with and without grade III/IVhypertensive retinopathy.Methods: A preplanned subanalysis of patients who presented to a university hospital ED with diastolic BP 120 mmHg and who enrolled in the Fundus Photography versus Ophthalmoscopy Trial Outcomes in the ED study was performed. Bilateral nonmydriatic ocular fundus photographs, vital signs, and demographics were obtained at presentation. Past medical history, laboratory values, healthcare utilization, and mortality were ascertained from medical record review at least 8 months after initial ED visit.Results: Twenty-one patients with diastolic BP 120 mmHg, 7 of whom (33%) had grade III/IV hypertensive retinopathy, were included. Patients with retinopathy were significantly younger than those without (median 33 vs 50 years, P ¼ 0.02). Mean arterial pressure (165 vs 163 mmHg) was essentially equal in the 2 groups. Patients with retinopathy had substantially increased but nonsignificant rates of ED revisit (57% vs 29%, P ¼ 0.35) and hospital admission after ED discharge (43% vs 14%, P ¼ 0.28). One of the patients with retinopathy died, but none without.Conclusion: Younger patients may be at higher risk for grade III/IV hypertensive retinopathy among patients with hypertensive urgency. Chronic compensatory mechanisms may have not yet developedin these younger patients. Alternatively, older patients with retinopathy may be underrepresented secondary to increased mortality among these patients at a younger age (survivorship bias). Further research is needed to validate these preli

Acute aortic syndrome is a pathological process with low incidence compared with acute coronary syndrome, although with a worse prognosis in the short term, which is why its early diagnosis and urgent treatment are essential to the favorable evolution of the patient. Electrocardiographic changes suggestive of myocardial ischemia, with acute evolution, are rare in acute aortic syndrome. Even in the presence of a suggestive thoracic pain and high levels of blood pressure, an adequate differential diagnosis is of utmost importance, since the administration of anticoagulation and antiplatelet therapy in high doses can have a dramatic impact on patient outcome. Two cases are presented in which electrocardiographic changes determined the action to take in patients with acute aortic syndrome Acute aortic syndrome, acute coronary syndrome, malignant hypertension., El síndrome aórtico agudo es un proceso patológico de baja incidencia en comparación con el síndrome coronario agudo, aunque con peor pronóstico a corto plazo, razón por la cual su diagnóstico precoz y tratamiento urgente son esenciales para la evolución favorable del paciente. Las alteraciones electrocardiográficas sugestivas de isquemia miocárdica, de evolución aguda, son poco frecuentes en el síndrome aórtico agudo, aunque en presencia de un dolor torácico sugestivo y cifras elevadas de presión arterial, un adecuado diagnóstico diferencial cobra suma importancia, ya que la administración de anticoagulación y antiagregación a altas dosis puede tener un impacto dramático en la evolución del paciente. Se presentan 2 casos clínicos en los que las alteraciones electrocardiográficas determinaron la conducta a seguir en pacientes con síndrome aórtico agudo.

Acute aortic syndrome is a pathological process with low incidence compared with acute coronary syndrome, although with a worse prognosis in the short term, which is why its early diagnosis and urgent treatment are essential to the favorable evolution of the patient. Electrocardiographic changes suggestive of myocardial ischemia, with acute evolution, are rare in acute aortic syndrome. Even in the presence of a suggestive thoracic pain and high levels of blood pressure, an adequate differential diagnosis is of utmost importance, since the administration of anticoagulation and antiplatelet therapy in high doses can have a dramatic impact on patient outcome. Two cases are presented in which electrocardiographic changes determined the action to take in patients with acute aortic syndrome Acute aortic syndrome, acute coronary syndrome, malignant hypertension., El síndrome aórtico agudo es un proceso patológico de baja incidencia en comparación con el síndrome coronario agudo, aunque con peor pronóstico a corto plazo, razón por la cual su diagnóstico precoz y tratamiento urgente son esenciales para la evolución favorable del paciente. Las alteraciones electrocardiográficas sugestivas de isquemia miocárdica, de evolución aguda, son poco frecuentes en el síndrome aórtico agudo, aunque en presencia de un dolor torácico sugestivo y cifras elevadas de presión arterial, un adecuado diagnóstico diferencial cobra suma importancia, ya que la administración de anticoagulación y antiagregación a altas dosis puede tener un impacto dramático en la evolución del paciente. Se presentan 2 casos clínicos en los que las alteraciones electrocardiográficas determinaron la conducta a seguir en pacientes con síndrome aórtico agudo.