Long-standing Hypertension Research Articles

Obstruction of the right coronary artery ostium due to acute aortic dissection

Acute aortic dissection presents with a wide range of manifestations and it is frequently confused with acute coronary syndrome, leading to delayed diagnosis and inappropriate treatment. A high clinical index of suspicion is necessary. Longstanding arterial hypertension, elevated D-dimer levels and new onset atypical chest pain can help the clinician to perform a difficult differential diagnosis. We present a case of acute aortic dissection in a 68-year-old Italian woman with longstanding arterial hypertension, unknown ascending aortic aneurysm, normal D-dimer levels, new onset atypical chest pain and electrocardiographic images mimicking acute coronary syndrome. Also this case focuses attention on the importance of a correct evaluation of new onset chest pain.

Vascular Stiffness and the “Chicken-or-the-Egg” Question

Although the incidence of hypertension approaches 90% for people over the age of 70 years, the etiology of hypertension remains elusive for the vast majority. The complications of long-standing hypertension are well known and relate to arterial disease with clinical manifestations in the heart, brain, and kidney. However, the paradigm of elevated blood pressure resulting in vasculopathy continues to be challenged. Rather than hypertension resulting in altered vascular structure and function, it seems that changes in vascular integrity (structure) precede and may be causal in the development of elevated blood pressure with resultant hypertension that ultimately leads to clinical events (Figure). Alterations in cardiovascular structure and function that have been shown to precede the finding of elevated blood pressure include the occurrence of left ventricular hypertrophy in children and young adults of hypertensive parents1 (although one cannot rule out the role of blood pressure in causing cardiovascular remodeling in studies where only resting, occasional measurements of blood pressure are made), diastolic filling abnormalities in normotensive individuals predisposed to hypertension,2 endothelial dysfunction as a precursor to the finding of hypertension,3 and increased arterial stiffness in normotensive subjects predisposed to develop hypertension.4 Recently it has …

Aortic Dissection and Third‐Degree Atrioventricular Block in a Patient With a Hypertensive Crisis

A 55-year-old man with a history of uncontrolled hypertension was admitted because of an episode of severely elevated blood pressure. An electrocardiogram revealed complete atrioventricular block while imaging showed a dissecting aneurysm of the descending thoracic and abdominal aorta, type B according to the Stanford classification. Laboratory tests revealed significant increases in serum C-reactive protein. Coronary arteriography was performed and was negative for coronary artery disease. A VDD pacemaker was placed, and a combination of 4 antihypertensive agents was used as treatment. Type B aortic dissection may present with a wide range of manifestations. The authors suggest that measurement of C-reactive protein may be used in hypertensive patients to help reflect vascular injury and its degree, progression, and prognosis. Disorders of intraventricular conductivity are rarely seen in both types of dissection of the aorta (type A, B). Atrioventricular conductivity disorders that result in complete atrioventricular block have been reported only in patients with type A dissection (before the bifurcation of the subclavian artery). In this particular case, however, the authors diagnosed an atrioventricular conductivity disorder causing atrioventricular block in a patient with type B dissection. Consequently, the authors speculate that myocardial fibrosis, as a result of long-standing hypertension, could be the main pathogenetic mechanism leading to the development of such phenomena, resulting from a potential expanding of the fibrotic process to the atrioventricular conduction system.

Pathogenesis of Elevated Peripheral Pulse Pressure

“Ashes to ashes, dust to dust, if the cancer don’t get us, the arteriosclerosis must” — —Richard Gordon in The Alarming History of Medicine, 1993 Substantial evidence suggests that arterial remodeling evolves over a life course under the conjoint influence of genes, environmental factors (including vascular risk factors), and lifestyle characteristics (such as diet and physical activity).1 Such arterial remodeling involves multiple vascular territories and is panarterial, ie, it involves all layers of the arterial wall.1 More recently, considerable attention has focused on the physiological aspects of propagation of blood within the aorta, and several important concepts have evolved. First, the aorta is no longer regarded as just a passive conduit that transports blood to the vital organs. Rather, it is a complex organ that remodels in dynamic fashion in response to biomechanical stresses that accumulate over the life course.1 The different segments of the aorta vary in their relations to risk factors, underscoring the heterogeneity in remodeling characteristics across the arterial tree.2 Second, age-associated changes in the aortic wall include fragmentation of the elastin fibers, increased synthesis of collagen, and calcification. The molecular epidemiology of these vascular remodeling changes have been well characterized, and are complex, being mediated via the interaction of vascular smooth muscle cells, integrins, metalloproteinases, endothelial function, and the renin-angiotensin axis, inflammation, and other pathways.1 Third, vascular flow propagation is the combination of steady flow (mean arterial pressure) and pulsatile (pulse pressure) components. The proximal (central) aorta stiffens with age, and these changes are associated with an increase in the pulsatile component (increased central pulse pressure), which in turn places a burden of increased afterload on the left ventricle. There is widespread agreement that elevated pulsatile load is associated with increased risk of cardiovascular disease, including myocardial infarction, stroke, and heart …

Emesis Following Ingestion of Race Car Fuel in a 7-Year-Old Male

3. Many pathological conditions contribute to elevated serum creatinine.1 Examples of pre-renal etiologies include volume depletion, massive hemorrhage, or systolic heart failure. Intrinsic renal diseases to consider include post-streptococcal glomerulonephritis, hemolytic uremic syndrome, and medication-induced interstitial nephritis or tubular necrosis. Post-renal etiologies, such as vesicoureteral reflux and kidney stones, should also be considered. Long-standing hypertension and diabetes mellitus are common etiologies of chronic renal failure, although these are unlikely causes in a pediatric patient. 4. Most likely diagnosis: False-positive creatinine value. Further investigation revealed that the race car fuel contained nitromethane. This product is reported to interfere with the Jaffe reaction for creatinine.

New guidelines for drive-by renal arteriography may lead to an unjustifiable increase in percutaneous intervention

Narrowing of the lumen of the renal artery is termed renal artery stenosis (RAS) and can be a cause of hypertension and chronic kidney disease (CKD).1 When hypertension is caused...

A 63-Year-Old Man With Multiple Cardiovascular Risk Factors and Poor Adherence to Treatment Plans

Mr P has long-standing hypertension, obesity, and diabetes mellitus and has experienced life-threatening cardiovascular events. Mr P is receiving evidence-based clinical care but has adhered to his medical regimen poorly and remains at considerable risk of future catastrophic cardiovascular events. Practicing evidence-based medicine should be a 5-step process: research uncovers the evidence, clinicians learn the evidence, clinicians use the evidence at every visit for every patient, clinicians make sure patients understand the evidence, and clinicians help patients incorporate the evidence into their lives. Research demonstrates, however, that clinicians do not use the evidence at every visit, patients may misunderstand what took place in the visit, and clinicians are not always effective in helping patients incorporate the evidence into their lives. These failures reflect the difficulty faced by clinicians attempting to address multiple issues while providing sufficient information and engaging in collaborative decision making during a brief clinical visit.

Hypertension, vascular cognitive disorders and neuroprotection.

The role of the antihypertensive therapy in preventing vascular cognitive disorders in elderly persons without a history of stroke is a matter of debate. This review focuses on cognitive disorders in elderly hypertensive patients. Relevant papers were identified by searches in PubMed from 1946 until February 2007 using the keywords 'cerebral blood flow autoregulation', 'vascular cognitive disorders', 'neuroimaging in hypertension', 'antihypertensive treatment' and 'neuroprotection in cerebral ischemia'. Excessive blood pressure lowering in patients with long-standing hypertension may increase the risk of cerebral hypoperfusion, white matter lesions and consequent cognitive decline. White matter lesions have been found in the majority of patients with long-standing hypertension. They correlate with vascular cognitive disorders, particularly impairments of attention and executive function, while memory is relatively preserved. Cerebral small vessel disease in elderly patients should be taken into account when antihypertensive treatment is considered. Renin-angiotensin blockade, some calcium channel blockers and statins are thought to possess neuroprotective action. For prevention of cerebral hypoperfusion in elderly hypertensives blood pressure lowering should be cautiously controlled. The increased risk of white matter lesions is an indication for early neuroprotection. The combination of renin-angiotensin blockade or calcium channel blockers with statins may become a promising preventive strategy against cognitive decline in elderly hypertensives. Cerebral white matter protection is a future challenge.

Équilibre de la balance hydrosodée et contrôle de la pression artérielle en DPA/DPCA

Cardiovascular disease remains the leading cause of death in ESRD patients undergoing Hemodialysis or Peritoneal Dialysis and a significant proportion of this is likely related to long-standing hypertension. Early studies had recognized the favourable effect of PD in controlling hypertension but it was soon realized that such benefit was not sustained. A U shaped trend of hypertension in patients on PD has been recently demonstrated as a result of a steadily increased blood pressure partly attributed to fluid retention resulting from lower sodium removal with time. Effort in selecting the best strategy of ultrafiltration for a single patient along with a carefull and frequent monitoring of combined 24 hours sodium elimination coupled with dietetician concelling can improve significantly fluid an sodium balance which in turn will result in much better blood pressure control. The contribution of progress in biocompatibility of PD fluid that better preserve renal function and the implementation of the first glucose polymer Icodextrin were key interventions in that aim. Further studies should be conducted to assess the power of innovative PD solutions — Low Sodium PDF and/or Bimodal Ultrafiltration — in enhancing fluid and sodium removal during CAPD/APD programmes.

Mice lacking sulfonylurea receptor 2 (SUR2) ATP-sensitive potassium channels are resistant to acute cardiovascular stress

Adenosine triphosphate-sensitive potassium (K ATP) channels are thought to mediate the stress response by sensing intracellular ATP concentration. Cardiomyocyte K ATP channels are composed of the pore-forming Kir6.2 subunit and the regulatory sulfonylurea receptor 2 (SUR2). We studied the response to acute isoproterenol in SUR2 null mice as a model of acute adrenergic stress and found that the episodic coronary vasospasm observed at baseline in SUR2 null mice was alleviated. Similar results were observed following administration of a nitric oxide donor consistent with a vasodilatory role. Langendorff-perfused hearts were subjected to global ischemia, and hearts from SUR2 null mice exhibited significantly reduced infarct size (54 ± 4 versus 30 ± 3%) and improved cardiac function compared to control mice. SUR2 null mice have hypertension and develop cardiac hypertrophy. However, despite longstanding hypertension, fibrosis was absent in SUR2 null mice. SUR2 null mice were administered nifedipine to block baseline coronary vasospasm, and hearts from nifedipine-treated SUR2 null mice exhibited increased infarct size compared to untreated SUR2 null mice (42 ± 3% versus 54 ± 3%). We conclude that conventional sarcolemmal cardiomyocyte K ATP channels containing full-length SUR2 are not required for mediating the response to acute cardiovascular stress.

Left Ventricular Remodeling Following Renal Transplantation

Background: Patients with chronic kidney disease frequently have left ventricular hypertrophy (LVH) related to long-standing hypertension. Diabetes, obesity and metabolic abnormalities also contribute to LVH. In these patients, renal transplantation ameliorates metabolic and electrolyte perturbations, interrupts renin – angiotensin - aldosterone system dysregulation and improves hypertension control. We hypothesized that these factors lead to favorable left ventricular remodeling and LVH regression.

Comparison of B-type natriuretic peptide with left atrial enlargement by echocardiography for the diagnosis of new-onset congestive heart failure with a preserved left ventricular systolic function in the setting of longstanding hypertension

The present study attempted to determine the accuracy of B-type natriuretic peptide (BNP) compared with left atrial enlargement at echocardiography in the emergency diagnosis of new-onset heart failure with preserved systolic function (HFPSF) related to longstanding hypertension. The study comprised 57 patients in sinus rhythm hospitalized for acute dyspnea, 30 with hypertensive HFPSF and 27 with noncardiac cause. By stepwise logistic regression analysis, BNP provided independent and incremental diagnostic information over the score of Boston criteria. There was a trend toward superiority of this biomarker compared to the left atrial area index for the diagnosis of HFPSF. A BNP concentration > 142 pg/ml was 93% sensitive and 85% specific for the diagnosis of HFPSF in this clinical setting (area under the ROC curve of 0.91 [0.8–0.97], p < 0.001).

Approach to patients with heart failure and pulmonary hypertension

Pulmonary hypertension (PH), defined as a mean pulmonary artery pressure greater than 25 mm Hg, is not a diagnosis, but rather the physiologic consequence of the interaction between pulmonary blood flow, pulmonary vascular impedance, and downstream pulmonary venous pressure. The diagnosis and appropriate treatment of PH in patients with or without heart failure (HF) requires an understanding of the underlying pathogenesis, whether it be due to increased pulmonary venous pressure, increased pulmonary vascular resistance (PVR), increased pulmonary blood flow, or a combination thereof. Furthermore, an explanation for the underlying cause must also be sought. For example, a rise in pulmonary venous pressure may relate primarily to an increase in left ventricular end-diastolic pressure in a patient with a known cardiomyopathy; however, it may be complicated by severe mitral regurgitation. Similarly, an increased PVR may reflect reactive changes in the pulmonary vasculature due to long-standing pulmonary venous hypertension, concomitant hypoxemia/hypercapnia, or it may be the harbinger of chronic thromboembolic disease. It is imperative that reversible causes of PH be considered. Although most often diagnosed by Doppler echocardiography, full hemodynamic characterization of PH requires right heart catheterization to measure biventricular filling pressures and PVR. Integration of invasive pulmonary hemodynamics with an assessment of right ventricular function is essential to appreciate the clinical and prognostic significance of PH of an individual patient. Right heart catheterization is not practically feasible in all patients with HF and PH; however, at a minimum it should be performed in patients with a Doppler-estimated pulmonary artery pressure greater than 60 mm Hg, those who present clinically with predominant right HF, significant mitral valve disease, and in particular, patients with impaired right ventricular function.

Nodular Glomerulosclerosis in the Nondiabetic Smoker

Emerging evidence supports that the entity known as idiopathic nodular glomerulosclerosis is not idiopathic. A strong causative association with longstanding cigarette smoking and hypertension has been identified. Morphologically, smoking-associated nodular glomerulosclerosis closely resembles diabetic nephropathy. The potential roles of advanced glycation end products, oxidative stress, angiogenesis, and hemodynamic perturbations are explored.

Acute poststaphylococcal glomerulonephritis superimposed on diabetic glomerulosclerosis

Acute poststaphylococcal glomerulonephritis superimposed on diabetic glomerulosclerosis

Experiences in the management of brainstem hematomas

The purpose of this study was to present our experience in the management of spontaneous brainstem hematomas (BSH). Records of 58 consecutive patients were reviewed, including demographic data, symptoms, Glasgow Coma Scale, treatment, intraoperative findings (in surgical cases), and outcome according to the Glasgow Outcome Scale. Fifteen patients were comatose (GCS 4 or less): 11/15 patients were treated conservatively. Four patients with accompanying acute occlusive hydrocephalus were treated by placement of an external ventricular drainage. None survived. In nine patients (60%), arteriosclerosis and/or long-standing arterial hypertension were known and arteriopathic BSH was suspected. Forty-three patients were not comatose: 37 patients showed no impairment of consciousness (GCS 15), 6 patients presented with mild disturbance of conscious state (GCS 13), progressing to coma (GCS 8) in 1. In the majority (36/43) of the non-comatose patients (83.7%) cavernoma could be revealed and removed surgically. In six patients (14%), an atypically located arteriopathic BSH was assumed and treated medically. One patient had an underlying brainstem arteriovenous malformation and was treated radiosurgically. Many arteriopathic BSH cause immediate coma indicating direct and irreversible damage of midpontine structures. Thus, we suggest not to proceed to surgery, even if the bleeding is accompanied by acute hydrocephalus. The majority of BSH not resulting in immediate coma are caused by underlying cavernomas. In these cases surgery should be considered.

Unstable single coronary artery

A 78-year-old male presented for elective cardiac catheterisation following a 1-week history of crescendo angina on a background of longstanding hypertension, hypercholesterolaemia, and transient ischaemic attacks. Cardiac catheterisation revealed a single coronary artery (SCA) anomaly, with the right coronary artery (RCA) arising from the right coronary sinus continuing on to sequentially form …

Ischemic preconditioning is lost in aging hypertensive rat heart: Independent effects of aging and longstanding hypertension

Although in experimental hypertension the cardioprotective effects of ischemic preconditioning (PC) appear to be maintained, most studies have examined the short-term hypertension in juvenile animals. However, aging may be an additional factor that influences the effectiveness of PC. The aim of this study was to characterise the effects on PC of LVH and aging simultaneously. Hearts from spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar–Kyoto rats (WKY) were studied. Excised hearts were Langendorff-perfused to give equivalent coronary flow per gram heart weight. The left main coronary artery was occluded for 35 min followed by 120 min reperfusion. Infarct size was determined by tetrazolium staining. Heart size was assessed as left ventricle/body weight ratio (LV/BW). PC was effected with 2 × 5 min periods of global ischemia prior to coronary occlusion. Hearts were studied at 3–4 months (juvenile), 7–8 months (mature) or 12–13 months (aging). LV/BW ratio in SHR increased relative to WKY controls by 20%, 32% and 40% in juvenile, mature and aging hearts, respectively, but ischemic risk zone size was similar in all groups (52–59% of LV). PC was equally effective at limiting infarct size in juvenile and mature SHR and WKY hearts but was ineffective in aging hearts from both WKY and SHR. Since angiotensin-converting enzyme inhibitors enhance sub-threshold PC in normal myocardium, we also examined the action of captopril (Cap) in aging hearts. Additional aging hearts received treatment with Cap 200 μM as an adjunct to PC. Although Cap + PC was able to induce modest protection in aging WKY hearts, this was not seen in aging SHR hearts. We conclude that PC is lost in longstanding hypertension through independent contributions of both hypertension and aging. These findings may have implications for the clinical development of preconditioning-based therapies since elderly patients with longstanding hypertension are at high risk of developing ischemic heart disease.

Invited commentary

Many patients presenting for cardiac surgery have significant left ventricular hypertrophy, commonly from long-standing hypertension or valvular heart disease. Several groups in the last 5 years have reported that left ventricular hypertrophy predicts excessive rates of morbidity and mortality in patients having cardiac surgery. Left ventricular hypertrophy is troublesome in that myocardial perfusion, particularly to the subendocardium, is not predictably homogenous. This issue becomes even more pertinent with coexisting coronary artery disease.

Ascending aorta dissecting aneurysm in a teenager with isolated systemic hypertension

A teenager with longstanding arterial hypertension was admitted for acute pneumonia treatment. New onset atypical chest pain for the last months and aortic valve regurgitation were also present. A dissecting aneurysm of the ascending aorta with moderate aortic valve regurgitation was evidenced by laboratorial diagnostic. Aneurismectomy with aortic valve preservation and coronary artery reimplantation was carried out.