Long-standing Hypertension Research Articles

A challenging triple valve surgery for long-standing pulmonary hypertension in rheumatic heart disease: a case report

Background Pulmonary hypertension is an increase in the mean pulmonary arterial pressure, greater than 25mmHg at rest, or greater than 30mmHg while exercising. In valvular heart disease its presence indicates a decompensated state of the disease. Surgical interventions are the ultimate treatment for the correction of valvular heart disease. Case Report A 38-year-old female was admitted to the Emergency Department (ER) with complaints of shortness of breath, chest pain, palpitations, and history of fainting. The patient was initially scheduled for aortic and mitral valve replacement and tricuspid valve repair at the end of year 2020. However, due to covid-19 pandemic, the patient was re-scheduled for surgery. On the 15th of June 2022, the patient was admitted to the ER of Zainoel Abidin General Hospital, and was consulted to the CTVS division. On the 17th of June 2022, the patient underwent a successful mitral valve replacement using mechanical St. Jude 29 mm valve, mechanical St. Jude 17 mm for aortic valve position, and tricuspid valve repair commissurotomy and using MC3 Edward ring annuloplasty. The patient was hospitalized for seven days and underwent successful first phase cardiac rehabilitation before discharge. The patient has since made remarkable improvements, establishing better quality of life. Conclusion Reduced pulmonary pressures postoperatively are often modest, and persistent pulmonary hypertension (PH) is known to be common and an indicator of poor prognosis. For patients with long-standing pulmonary hypertension due to rheumatic heart disease, valve replacement surgery effectively reduces pulmonary hypertension caused by damage to the left heart valve.

S-03-1: BRAIN IMAGING FOR THE MANAGEMENT OF HYPERTENSION

Small vessels in the brain is susceptible especially for the effect of hypertension. Therefore, longstanding hypertension may induce cerebral small vessel disease (CSVD) which is designated as hypertensive CSVD. The patients with hypertensive CSVD may exhibit various types of lesions including lacunar infarction, white matter lesion, cerebral hemorrhage and microbleeds in brain magnetic resonance (MR) imaging. White matter lesions (WMLs) are one of the most representative lesions which are closely related to hypertension and aging. They are classified into periventricular hyperintensity (PVH) and deep white matter hyperintensity (DWMH), and the former is more closely involved in cognitive decline than the latter. In the SPRINT MIND trial which examined the significance of intensive blood pressure control, WML volume increased by 0.28 cm3 for 4years in the intensive treatment group whereas by 0.92 cm3 in the standard treatment group, indicating 70% suppression of WML expansion. We quantitatively assessed WML volume in patients with vascular dementia and Alzheimer disease, and as expected, both PVH DWMH were significantly larger in vascular dementia than in Alzheimer disease. The mechanisms for CMBs are not fully understood but may be secondary to blood-brain barrier damages from long-standing hypertension, or alternatively, amyloid deposition in the tissue. In our previous study, we investigated degree of SVD changes using hypertensive arteriopathy SVD (HA SVD) and cerebral amyloid angiopathy SVD (CAA SVD) scores. With the analysis of SVD scores in 53 subjects with CMBs admixed with lobar and deep distributions, mixed CMBs were mainly caused by HA. These neuroimaging markers are crucial for management of hypertension. Small subcortical stroke (SPS3) trial which enrolled patients with symptomatic lacunar infarctions, were divided into two groups: those with a systolic blood pressure target between 130 and 149 mm Hg and those with less than 130 mm Hg. There was no significant difference in the frequency of all strokes, the rate of intracerebral hemorrhage was significantly lower in the group with intensive blood pressure control. This SPS3 trial revealed that a systolic blood pressure target of less than 130 mm Hg is beneficial in reducing risk in lacunar stroke patients. Thus, we overview brain imaging markers in hypertensive patients and their significance for the management of SVD.

Assessment of Knowledge, Attitudes and Practices Regarding Chronic Kidney Disease in at-Risk Individuals

Background: Chronic kidney disease (CKD) is a global health problem, with a worldwide prevalence of around 9.1 per cent (as of 2017). In India, its prevalence was found to be around 17.2%. There are several risk factors of CKD, out of which the presence of underlying longstanding uncontrolled diabetes mellitus (DM) and hypertension are common. Certain previous studies have tried to assess the level of knowledge, attitudes and practices of such a ‘high risk’ group for developing CKD but there is a paucity of literature on it. Hence, this study was undertaken to assess these domains in individuals at risk for developing CKD. Patients and Methods: It is an observational cross-sectional study conducted from October 2020 to December 2021 at a tertiary care teaching and referral hospital in India. A total of 215 patients who were at risk of developing CKD, were enrolled and were given a CKD Screening Index questionnaire to fill and scoring was done for all three components-knowledge, attitudes and practices. Results: The mean age was found to be 49.21 ± 13.49 years with a male: female ratio of 1.4:1. Nearly three-a fourth of the patients were having DM while one-fourth of the participants had a previous history of hypertension. The mean scores on the knowledge, attitude and practices scales were found to be 11.80 ± 5.31, 50.18 ± 8.23 and 30.83 ± 7.53 respectively. The study results revealed that the majority of patients had ‘low’ levels of knowledge scores but ‘average’ levels of attitude and practice scores. A significant correlation was found amongst knowledge and attitude scores (r = 0.226, P = 0.001), knowledge and practice scores (r = 0.153, P = 0.025) and practice and attitude scores (r = 0.295, P = 0.000) of our patients. Conclusion: There is a need of improving awareness at least amongst the population at risk of getting CKD. Improving knowledge would help in inculcating positive attitudes and healthier practices amongst these, thus delaying the onset of this disease.

A rare case of eisenmenger syndrome in a young nigerian male with an undiagnosed atrial septal defect

Eisenmenger syndrome refers to the reversal of an original left-to-right shunt due to long-standing pulmonary hypertension and high pulmonary vascular resistance, in the presence of an intracardiac anatomic defect. Few cases have been reported in Nigeria. The importance of early identification of a cardiac defect cannot be overemphasized, as this leads to avoidance of pulmonary vascular disease (which can impact morbidity and mortality) by repairing the defect. We report a case of an adult male presenting with shortness of breath due to atrial septal defect causing pulmonary arterial hypertension with Eisenmenger physiology, to highlight the occurrence of this rare condition in our locality, to raise awareness for a high index of suspicion.

A Case of Orthotopic Renal Transplant in a Patient with Diffuse Atherosclerosis

A 60-year-old male with long-standing diabetes, hypertension, and smoking developed an end-stage renal disease that necessitated hemodialysis. His drive-by angiograms revealed significant carotid and iliac calcifications and a triple-vessel disease on cardiac assessment. The abdominal aorta, common iliac, and the vascular tree below were all heavily calcified, according to a computed tomography angiography. Concerned about the location of the donor renal artery anastomosis, the decision was taken to do a left native kidney nephrectomy and orthotopic renal transplant. End-to-end anastomoses were made between the donor renal artery and splenic artery and between the donor renal vein and the recipient native kidney renal vein. The patient is doing well after the transplant, and the graft is functioning excellently with a creatinine of 0.9 mg/dl.

Correlation between coronary artery calcium score and aorta diameter in population with long-standing hypertension using noncontrast CT scan

Background: Early detection of aortic aneurysms is challenging in hypertensive patients due to the high risk of life-threatening ruptures. Limited studies on the relationship between coronary artery calcium and aortic diameter are present. This study evaluated the correlation between coronary artery calcium score (CACS) and maximal thoracic and abdominal aortic diameters in hypertensive patients, using a noncontrast CT scan. Material and methods: We prospectively enrolled 180 hypertensive patients older than 45 who had no aortic aneurysm or heart disease. We split the study population into five classes according to CACS (0, 1–10, 10–100, 100–400, and > 400). We calculated coronary artery calcium and maximal diameters of the ascending thoracic aorta (ATAMAX), descending thoracic aorta (DTAMAX), and abdominal aorta (AAMAX) using native computed tomography imaging. Results: Coronary artery calcium score was high in patients with high abdominal aorta diameter but not with the high diameters of the thoracic aorta. The cut-off point of the abdominal aorta’s maximum diameter was 34 mm, so AAMAX > 34 mm is predictive of a diagnosis of CACS category five (CACS > 400). There were no differences in ascending and descending thoracic aorta measurements between patients with a coronary artery calcium score of more than 400 (category 5) and the rest. Conclusion: Screening for an abdominal aortic aneurysm is essential in hypertensive patients as the coronary artery calcium score is associated significantly with increased abdominal aorta diameter. However, the necessity for thoracic aortic aneurysm screening is not apparent in these patients as no significant association is found between CACS and thoracic aorta diameter.

A Case of Spinal Cord Injury Caused By Electrical Stimulation of Thoracic Spinal Cord for Treatment of Diabetic Foot

The thoracic Spinal Cord Stimulator (SCS) has been widely accepted as a treatment option for diabetic foot and is gaining acceptance. This case highlights a previously unreported potential complication of the SCS. A 66-year-old man had long-standing diabetes (30 years) and hypertension (10 years), accompanied by diabetic foot and generalized psoriasis. The patient reported pain in the bilateral lower extremities, especially in both feet, which was significant at night and when walking. His Visual Analog Scale (VAS) pain score was 10/10. The pain was accompanied by slight numbness without sensory disturbance. These symptoms gradually exacerbated over 2 months. His Quality of Life Scale (QOLS) score was 186, and the skin temperature of both his feet decreased at rest. Following conservative treatment elsewhere, the abovementioned symptoms remained refractory; the patient presented to our hospital for further treatment. SCS was implanted on June 6, 2021 for pain relief.

#1321314: Primary Hyperaldosteronism Diagnosed in a 58-Year-Old Male with Longstanding Hypertension and Hypokalemia: A Case Highlighting the Importance of Early Screening and Appropriate Care of Primary Aldosteronism for Longstanding Resistant Hypertension and Hypokalemia

Primary aldosteronism (PA) is caused by autonomous secretion of aldosterone by the adrenal glands. PA is the most common cause of secondary hypertension and accounts for about 20% of cases among patients with resistant hypertension.

Abstract 14746: Pulse Pressure More Strongly Associates With Subclinical Myocardial Injury Than Do Systolic and Diastolic Blood Pressures

Introduction: Long-standing hypertension is associated with subclinical myocardial injury expressed as chronically elevated cardiac troponin concentrations. Subclinical myocardial injury and subsequent diffuse myocardial fibrosis may represent important intermediaries between hypertension and risk of heart failure and cardiovascular (CV) death. The relative strength of the associations between systolic blood pressure (BP), diastolic BP and pulse pressure and subclinical myocardial injury is unknown. Aim: To assess the relative impact of systolic BP, diastolic BP and pulse pressure on subclinical myocardial injury. Methods: Cardiac troponin I (cTnI) was measured by a high-sensitivity assay (Abbott Diagnostics) in 32,968 participants of the fourth wave of the Trøndelag Health Study (HUNT4) from 2017 to 2019. The longitudinal substudy included participants from HUNT4 who also had BP measurements from the third wave of HUNT (HUNT3) from 2006 to 2008. This included 18,681 study participants. All study participants with a history of CV disease were excluded prior to analysis. We defined subclinical myocardial injury as cTnI ≥4ng/L for women and ≥6ng/L for men, and used logistic regression models adjusted for established CV risk factors. Results: The mean age was 52 (SD±17) years, and 56.9% were female. Cross-sectionally, pulse pressure was more strongly associated with subclinical myocardial injury (adjusted odds ratio [aOR] 1.08, 95% confidence interval [CI] 1.06-1.10) compared to systolic BP (aOR 1.05, 95% CI 1.04-1.06) and diastolic BP (aOR 1.02, 95% CI 0.99-1.04). Longitudinally, change in diastolic BP was the only BP variable associated with subclinical myocardial injury (aOR 1.03, 95% CI 1.01-1.06), compared to change in systolic BP (aOR 1.01, 95% CI 0.99-1.02) and change in pulse pressure (aOR 0.99, 95% 0.97-1.01, p for all comparisons < 0.05). Conclusions: At a given time, pulse pressure is the superior BP variable in predicting subclinical myocardial injury. Over time, only change in diastolic BP is associated with subclinical myocardial injury. High pulse pressure and longitudinal changes in diastolic BP could represent hypertension phenotypes at high risk for subclinical myocardial injury and subsequent increased CV risk.

LBSAT61 Pure Aldosterone-secreting Adrenocortical Carcinoma Causing Resistant Hypertension In A Patient With Previously Controlled Longstanding Hypertension: A Case Report

Abstract Introduction Adrenocortical carcinoma is a rare endocrine malignancy that could be classified into functioning or non-functioning, depending on the tumor's ability to secret adrenocortical hormones. Pure aldosterone-secreting adrenocortical carcinoma is extremely rare, accounting for <7% of all functioning tumors that could present with primary aldosteronism and secondary hypertension. Case Presentation A 48-year-old man had a past medical history of longstanding hypertension that recently became resistant to multiple antihypertensive medications (thiazide, angiotensin receptor inhibitor, calcium channel blocker, hydralazine) despite medications compliance. He presented to the ER with left flank pain that was not associated with dysuria, nausea, or vomiting. On admission, his blood pressure was 223/135 mmHg. CT scan of the abdomen and pelvis showed mild left-sided hydronephrosis, hydroureter with a 2mm stone at the left ureterovesical junction, and a 7. 0×7. 0×6.4 cm left heterogeneous adrenal mass that was highly suspicious for malignancy. His laboratory workup revealed low serum potassium of 2.9 mmol/L (reference value 3.5-5.1 mmol/L), serum creatinine of 1.38 mg/dL (reference value 0.7-1.3 mg/dL), random cortisol of 21.8 mcg/dL (reference value 5-25 mcg/dL), ACTH of 5 pmol/L (reference value 10-60 pmol/L), serum levels of normetanephrine of 0.67 nmol/L (reference range 0-0.89 nmol/L), metanephrines of <0.10 nmol/L (reference range 0-0.49 nmol/L), and chromogranin A of 45 ng/mL (reference range 0-95 ng/mL). Further investigations showed high serum aldosterone of 28 ng/dL (reference range 2-9 ng/dL) and low plasma renin activity of 0.1 ng/mL per h (reference range 0.5-2.5 ng/mL per h) supported the diagnosis of primary aldosteronism. The patient underwent left adrenalectomy, and the diagnosis of pure aldosterone-secreting adrenocortical carcinoma was confirmed by histological examination. Conclusion Pure aldosterone-secreting adrenocortical carcinoma is an extremely rare adrenal tumor that could cause resistant hypertension. Re-evaluation of secondary causes of hypertension is essential in patients with a previously controlled longstanding hypertension, developing uncontrolled or resistant hypertension. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

ODP051 Presymptomatic Genetic Screening Leading to the Diagnosis of Paraganglioma Associated with Duodenal and Pancreatic Neuroendocrine Tumours in a Carrier of a Pathogenic MAX Variant

Abstract Introduction MAXpathogenic variants have been found to predispose to pheochromocytomas and paragangliomas (PPGLs) and more recently to pituitary tumors 1. Clinical Case A 30 yo man presented to the emergency department for diplopia and high blood pressure (200/100mmHg). His workup showed elevated plasmatic normetanephrines (9. 01nmol/L; N <0.92) and a 3.7cm right adrenal mass with a density of 30HU. The patient underwent right laparoscopic adrenalectomy and the pathologist reported a 4.5cm pheochromocytoma with a PASS score of 4 and a Ki-67 of 2-4%. The patient was screened with a panel of 14 susceptibility genes for PPGLs (INVITAE, CA, USA) that revealed a pathogenic germline nonsense heterozygous MAX mutation (c.223C>Tp. Arg75*). This mutation was previously described in a family where four members suffered from bilateral PHEOs at a young age (28-35 yo) 2 . Following the identification of the pathogenic variant of MAX gene, the patient's father (61 yo) underwent genetic counselling and was found to carry the same germline mutation. His past medical history included long-standing hypertension with hypertensive cardiomyopathy and diabetes. His blood work showed a mildly elevated plasmatic normetanephrine (1.41nmol/L; N <1.2) with normal metanephrine. An abdominal CT-scan showed a 1.5cm precaval nodularity. On a complementary 18 F-FDG PET/CT, the precaval mass had a 3.5 SUVMax and a second mass was identified in the duodenum (D3) with an uptake of 4.9 SUVMax. The 68 GaDOTATE PET/CT confirmed the precaval (SUVMax36.3) and duodenal (SUVMax51.6) lesion and in addition, revealed a pancreatic mass (SUVMax9.3). The patient underwent a distal pancreatic, duodenal and precaval node resection. The pathology report showed a 1.7cm G1 pancreatic neuroendocrine tumor (NET) (Ki-67 <3%) and a 2.3cmG1 duodenal NET (Ki-67 <3%). The precaval node was a paraganglioma (PGL) with a preserved SDHB staining, negative cytokeratine 8/18 and a Ki-67 of 1.65%. The son had normal imaging of his pancreas. To our knowledge we report the second case of association of MAXmutation with gastrointestinal TNE. Conclusion This case presents the rare association of a familial MAX mutation presenting with a pheochromocytoma in the index case and a presymptomatic discovery of a PGL and multiple NETs in the father. This supports the hypothesis that MAXmutations might be associated with multiendocrinetumors 3.

S2438 A Rare Cause of Esophageal Varices

Introduction: Esophageal varices (EV) are classified as downhill or uphill varices. Uphill varices are common and found in the distal esophagus that develop secondary to portal hypertension. Downhill esophageal varices (DEV) are rare and found in the proximal and mid esophagus and most commonly develop from obstructed venous blood flow in the superior vena cava (SVC). Case Description/Methods: A 74-year-old White male with past medical history of ESRD who was on hemodialysis for 5 years before a renal transplant was performed, COPD Gold Stage II, and obstructive sleep apnea presented to clinic with weight loss and dysphagia for the past year. The patient had no history of liver disease, physical examination was unremarkable, and his labs were normal. An esophagogastroduodenoscopy (EGD) revealed one large non-bleeding esophageal varix (EV) in the mid-esophagus and whitish plaques later confirmed by pathology to be Candida esophagitis. The patient was placed on IV micafungin and his dysphagia resolved. A CT Abdomen showed a normal liver and spleen. To further assess the DEV, a CT angiogram of the chest was obtained and revealed significant narrowing of SVC. (Figure). To evaluate the cause of SVC stenosis, an echocardiogram was ordered which revealed moderate to severe dilation of the right ventricle and evidence of pulmonary hypertension deemed to be likely secondary to his COPD and OSA. Of note, the patient had a prior chronic hemodialysis (HD) indwelling catheter in his SVC. After discussion with cardiology and CT surgery, the patient was referred to cardiology for an SVC venogram and right heart catheterization to measure pulmonary pressures. Discussion: DEV are formed when there is an obstruction in the SVC causing retrograde blood flow into the right atrium through collateral channels. The proximal and mid esophageal veins drain into the collaterals and the increased pressure result in DEV. The most common etiology is thrombosis of the SVC, but DEV can also be caused by severe pulmonary hypertension, thyroid tumors, and complications with HD catheters. In our case, the patient’s prior chronic HD catheter likely caused narrowing of the SVC lumen, along with long-standing pulmonary hypertension. Currently, there are no guidelines for screening or management of DEV. Physicians should be aware of unusual causes of varices and the management of DEV involves a multidisciplinary approach to treat the underlying cause of the SVC obstruction.Figure 1.: Significant narrowing of SVC (red arrow) on CT chest.

Postmenopausal hyperandrogenism due to an ovarian sex cord-stromal tumour causing elevated dehydroepiandrosterone sulphate: a case report

BackgroundThe source of excess androgen can be obscure in postmenopausal women with new-onset hyperandrogenism. If serum dehydroepiandrosterone sulphate (DHEAS) is raised, it is presumed to be of adrenal origin because DHEAS is exclusively produced from adrenal cortical cells. This reports an elderly female presenting with new-onset hyperandrogenism due to an ovarian sex cord-stromal tumour, associated with increased serum DHEAS levels.Case descriptionA 76-year-old female with long-standing diabetes and hypertension presented with hirsutism and male type alopecia for six months. She had menopause at 55 years of age. There was a pelvic mass on examination. Total testosterone was 6.106 ng/ml (0.124–0.357) and DHEAS was > 1000 µg/dL (35–430). Contrast-enhanced computed tomography of the abdomen and pelvis showed a heterogeneously enhancing complex mass measuring 11 × 8 cm in the left adnexal region. Adrenal glands were normal. She underwent total abdominal hysterectomy, bilateral salphingo-oophorectomy, and omentectomy. Both testosterone and DHEAS normalised following surgery. Histology revealed a sex cord-stromal tumour, likely a steroid cell tumour with malignant potential. Fluorodeoxyglucose-Positron emission tomography did not show any additional lesions.ConclusionsDue to the lack of sulfotransferase in ovarian tissue, markedly elevated DHEAS originating from an ovarian neoplasm is unusual. This phenomenon has not been described except in a patient with a steroid cell tumour causing Cushing syndrome and hyperandrogenism. The mechanism of this rare occurrence remains elusive. Knowledge of this unusual presentation would enable the clinicians to be cautious in localising the androgen source in women with hyperandrogenism.

Daily blood pressure profile and blood–brain barrier permeability in patients with cerebral small vessel disease

Cerebral small vessel disease (CSVD) plays an important role in cognitive impairment, stroke, disability, and death. Hypertension is the main risk factor for CSVD. The use of antihypertensive therapy has not resulted in the expected decrease in CSVD complications, which may be related to the underestimation of significance of daily blood pressure profile for blood–brain barrier (BBB) permeability. 53 patients with CSVD of varying severity (mean age 60.08 ± 6.8 years, 69.8% women, subjects with treated long-standing hypertension vs. normotensive subjects − 84.8% vs. 15.2%) and 17 healthy volunteers underwent ambulatory blood pressure monitoring (ABPM) and MRI, including T1-weighted dynamic contrast-enhanced magnetic resonance imaging for assessing BBB permeability. Most of ABPM parameters in CSVD patients did not differ from controls, but were associated with the severity of white matter hyperintensity (WMH) and the total CSVD score. BBB permeability in normal-appearing white matter (NAWM) and grey matter (GM) was significantly higher in CSVD patients, and the severity of BBB permeability remained similar in patients with different stages of WMH. Among BBB permeability parameters, the area under the curve, corresponding to an increase in the contrast transit time in NAWM, had the greatest number of correlations with deviations of ABPM parameters. BBB permeability in CSVD is a universal mechanism of NAWM and GM damage associated with a slight increase in ABPM parameters. It is obvious that the treatment of hypertension in patients with not severe WMH should be more aggressive and carried out under the control of ABPM.

Involvement of Lysyl Oxidase in the Pathogenesis of Arterial Stiffness in Chronic Kidney Disease

RationaleIncreased vascular stiffness is a key mediator of cardiovascular disease (CVD) in patients with chronic kidney disease (CKD). Increased vascular stiffness in CKD is thought to be the consequence of long‐standing hypertension and vascular calcification. However, vascular stiffness is increased early in patients with CKD, even before metabolic complications develop. Lysyl Oxidase (LOX) is a key mediator of collagen crosslinking and matrix remodeling. Up‐regulation of LOX has been associated with increased tissue stiffness in cancer and wound healing. We hypothesize that increased LOX might be a key mechanism for increased vascular stiffness in CKD. β‐aminopropionitrile (BAPN), a LOX inhibitor, was used to test the hypothesis.Methods5/6 nephrectomy (Nx) or Sham surgery was performed in 8‐weeks old male C57BL/6 mice. 2‐weeks after Nx, mice were randomized to BAPN (300 mg/kg/day in water) or vehicle for 4‐weeks. Vascular stiffness was assessed by pulse wave velocity (PWV). LOX levels were measured by ELISA and qPCR. Collagen crosslinking was measured by mass spectrometry. Comparisons between groups were made using one‐way ANOVA, p‐Value <0.05 was accepted as significant.ResultsNx resulted in decreased renal function at 8 weeks but no change in blood pressure or calcification. (~2‐3‐fold increase in creatinine, urea, and cystatin C) compared to control mice. Nx surgery resulted in increase in PWV (Con:179±32, Nx: 306 ± 47 cm/s, p<0.001). This was associated with an increased LOX in aorta (Con:118±8, Nx: 311±13 pg/mg dry weight, p<0.001). Mice with Nx surgery had an increased total collagen contents (183%, p<0.001) as well as cross‐linked collagen (DPD; 83%, p<0.05, PYD: 270% p<0.01). BAPN treatment significantly attenuates PWV (211± 49 cm/s, p<0.01), LOX (256±21 pg/mg dry weight, p<0.05) and total collagen contents (23%, p<0.01). BAPN treatment reduced the crosslinked collagens (DPD and PYD) but this did not reach statistical significance.ConclusionOur findings suggest: a) Increased vascular stiffness in CKD is independent of BP and calcification b) LOX mediated changes in extracellular matrix are at least in part responsible for the pathogenesis of arterial stiffness in CKD. Inhibition of excessive LOX may have therapeutic potential in alleviating increased vascular stiffness in CKD.

The Diagnostic Value of Combined 24-h BP and ECG Holter Monitoring in Detection of Cardiac Arrhythmias in Patients with Arterial Hypertension.

Background:Arrhythmias are common problems in hypertensive patients. The presence and complexity of both supraventricular and ventricular arrhythmias may influence morbidity, mortality, as well as the quality of life of patients.Objective:The aim of this study was to assess the diagnostic value of combined 24h BP and ECG Holter monitoring in detection of cardiac arrhythmias in patients with arterial hypertension.Methods:We analyzed the simultaneous records of combined 24h BP and ECG Holter monitoring for 356 adult patients with diagnosed arterial hypertension in the period from January 2017 until January 2021 year. The cardiac arrhythmias were classified in three main groups as following: a) Supraventricular arrhythmias; b) Ventricular arrhythmias; c) Bradyarrhythmia’s. Standard transthoracic echocardiograms were performed in order to evaluate signs of hypertensive or structural heart disease with focus on left ventricle hypertrophy and LV function.Results:Patients had a mean age of 64 ± 11years, 62% male. Average clinic BP was 153.4+18/87.5+14 mmHg. More than 46% of patients displayed a very high-risk profile. In all enrolled patients, cardiac arrhythmia was detected in 302 (84%) patients. The total number of patients with supraventricular arrhythmias was 153 (50,7%). Ventricular arrhythmias were detected in 98 (32,5%) patients. Bradyarrhythmia’s were detected in 51 (16,9%) patients. Elevated resting heart rate in sinus rhythm was detected in 87 (31,6%) of 275 patients with sinus rhythm.Conclusion:Most arrhythmias are related to longstanding arterial hypertension. Effective treatment of arterial hypertension plays important role in preventing structural and functional cardiac abnormalities which will contribute to the reduction of cardiac arrhythmias in hypertensive patients.

Juxtaglomerular cell tumour of the kidney: a rare cause of resistant hypertension.

SummaryJuxtaglomerular cell tumour (JGCT) is an unusually encountered clinical entity. A 33-year-old man with severe long-standing hypertension and hypokalaemia is described. The patient also suffered from polyuria, polydipsia, nocturia and severe headaches. On admission, laboratory investigation revealed hypokalaemia, kaliuresis, high aldosterone and renin levels, and the abdomen CT identified a mass of 4 cm at the right kidney. Kidney function was normal. Following nephrectomy, the histological investigation revealed the presence of a JGCT. Immunostaining was positive for CD34 as well as for smooth muscle actin and vimentin. Following surgery, a marked control of his hypertension with calcium channel blockers and normalization of the serum potassium, renin or aldosterone levels were reached. According to our findings, JGCT could be included in the differential diagnosis of secondary hypertension as it consists of a curable cause. The association of JGCT with hypertension and hypokalaemia focusing on the clinical presentation, diagnostic evaluation and management is herein discussed and a brief review of the existing literature is provided.Learning pointsJuxtaglomerular cell tumours (JGCT), despite their rarity, should be included in the differential diagnosis of secondary hypertension as they consist of a curable cause of hypertension.JGCT could be presented with resistant hypertension along with hypokalaemia, kaliuresis and metabolic alkalosis. Early recognition and management can help to prevent cardiovascular complications.Imaging (enhanced CT scans) may be considered as the primary diagnostic tool for the detection of renal or JGCT.For the confirmation of the diagnosis, a histopathologic examination is needed.

Late presentation of middle aortic syndrome complicated with severe aortic regurgitation; the role of endovascular intervention as a bridging for Bentall surgery

Middle aortic syndrome presents with segment narrowing of the descending thoracic and abdominal aorta. A common manifestation is uncontrolled hypertension, which can lead to severe aortic regurgitation in the long term. We have presented the case of a 31-year-old woman with worsening heart failure symptoms and longstanding uncontrolled hypertension. Echocardiography revealed severe aortic regurgitation. Aortic computed tomography showed severe stenosis of the aorta at the diaphragm level. Stent graft implantation was performed, followed by Bentall surgery 1 year later. Endovascular stent graft implantation of the descending aorta can be used safely as a bridging surgery for the Bentall procedure to reduce the patient’s blood pressure and relieve heart failure symptoms.

Heart-Brain Relationship in Stroke.

The patient presenting with stroke often has cardiac-related risk factors which may be involved in the mechanism of the stroke. The diagnostic assessment is predicated on recognition of this potential relationship. Naturally, an accurate history is of utmost importance in discerning a possible cause and effect relationship. The EKG is obviously an important clue as well as it allows immediate assessment for possible cardiac arrhythmia, such as atrial fibrillation, for possible acute ischemic changes reflective of myocardial ischemia, or there may be indirect factors such as the presence of left ventricular hypertrophy, typically seen with longstanding hypertension, which could be indicative of a hypertensive mechanism for a patient presenting with intracerebral hemorrhage. For all presentations in the emergency room, the vital signs are important. An elevated body temperature in a patient presenting with acute stroke raises concern about possible infective endocarditis. An irregular–irregular pulse is an indicator of atrial fibrillation. A markedly elevated blood pressure is not uncommon in both the acute ischemic and acute hemorrhagic stroke setting. One tends to focus on possible cardioembolic stroke if there is the sudden onset of maximum neurological deficit versus the stepwise progression more characteristic of thrombotic stroke. Because of the more sudden loss of vascular supply with embolic occlusion, seizure or syncope at onset tends to be supportive of this mechanism. Different vascular territory involvement on neuroimaging is also a potential indicator of cardioembolic stroke. Identification of a cardiogenic source of embolus in such a setting certainly elevates this mechanism in the differential. There have been major advances in management of acute cerebrovascular disease in recent decades, such as thrombolytic therapy and endovascular thrombectomy, which have somewhat paralleled the advances made in cardiovascular disease. Unfortunately, the successful limitation of myocardial damage in acute coronary syndrome, with intervention, does not necessarily mirror a similar salutary effect on functional outcome with cerebral infarction. The heart can also affect the brain from a cerebral perfusion standpoint. Transient arrhythmias can result in syncope, while cardiac arrest can result in hypoxic–ischemic encephalopathy. Cardiogenic dementia has been identified as a mechanism of cognitive impairment associated with severe cardiac failure. Structural cardiac abnormalities can also play a role in brain insult, and this can include tumors, such as atrial myxoma, patent foramen ovale, with the potential for paradoxical cerebral embolism, and cardiomyopathies, such as Takotsubo, can be associated with precipitous cardioembolic events.

Transient Cardiac Rhythm Changes.

Scenario: The 2 rhythm strips shown here (approximately 18 minutes apart) are from a 76-year-old woman admitted to the cardiac telemetry unit for exacerbation of heart failure. The patient’s history includes hypertension, type 2 diabetes, diastolic heart failure due to long-standing hypertension, and an atrioventricular (AV) pacemaker. The patient is resting comfortably in bed and is scheduled for discharge in the late afternoon. Given the rhythm strips, is it safe to discharge the patient?Normal sinus rhythm with possible right atrial enlargement and secondary repolarization changes. There is intermittent AV paced rhythm with appropriate AV sensing and pacing.A 3-letter code is used to describe the type of pacing used. The first letter denotes the chamber paced: A = atrium, V = ventricle, D = dual (ie, both A and V). The second letter denotes the chamber sensed, using the same nomenclature. Sensing inhibits pacing when an intrinsic P wave and/or QRS complex is present. The third letter denotes the response to sensing: I = inhibit, T = triggered, and D = dual function. In the top electrocardiography (ECG) strip, atrial activity is sensed (consistent P waves); thus, atrial pacing is inhibited. However, after the seventh P wave, an intrinsic QRS complex does not occur for >22 milliseconds, which triggers ventricular pacing. In the bottom strip, just after the ventricular paced beat, a P wave is not sensed and atrial pacing occurs. However, an intrinsic QRS complex occurs after atrial pacing, thus inhibiting ventricular pacing. By the sixth beat, both P waves and QRS complexes are sensed, thus inhibiting both atrial and ventricular pacing. This pattern suggests that the patient’s pacemaker is DDD. Moreover, the asymmetric biphasic P waves suggest atrial enlargement. Given that the impulse propagates from right to left atrium, a larger initial P compared with the terminal P’ suggests that the right chamber is the one enlarged. The T-wave inversion in lead II is most likely secondary repolarization changes due to diastolic dysfunction and right ventricular hypertrophy (cor pulmonale), consistent with the patient’s history. Verify with a 12-lead ECG and/or echocardiogram if available.The development of the first-degree AV block is the reason that transient pacing occurs. Medications (ie, β-blockers and/or digoxin) are a potential source of the problem, so medications in use should be evaluated as a possible cause and adjusted accordingly. Digoxin blood levels would be helpful; however, this patient is not taking digoxin. This patient’s DDD pacer is functioning properly; hence, no intervention is necessary and the patient can be discharged home.