Hypertensive Cardiac Failure Research Articles

Ginsenoside Rg5 alleviates Ang II–induced cardiac inflammation and remodeling by inhibiting the JNK/AP-1 pathway

Increased level of Angiotensin II (Ang II) contributes to hypertensive heart failure via -hemodynamic and non-hemodynamic actions. Ginsenoside Rg5 (Rg5) occurs naturally in ginseng, which has shown various benefits for cardiovascular diseases. This study evaluated Rg5′s effects on Ang II-caused cardiac remodeling and heart failure. C57BL/6 mice developed hypertensive cardiac failure after four weeks of Ang II infusion. The mice were administered Rg5 via oral gavage for the last two weeks to investigate the potential mechanism of Rg5. RNA sequencing of heart tissues was performed for mechanistic studies. It was discovered that Rg5 inhibited cardiac inflammation, myocardial fibrosis, and hypertrophy, and prevented cardiac malfunction in mice challenged with Ang II, without altering blood pressure. RNA sequencing showed that Rg5′s cardioprotective effect involves the JNK/AP-1 signaling pathway. Rg5 diminished inflammation in mice hearts and cultured cardiomyocytes by blocking Ang II-activated JNK/AP-1 pathway. In the absence of JNK or AP-1 in cardiomyocytes, the anti-inflammatory effects of Rg5 were nullified. The study found that Rg5 preserved the hearts of Ang II-induced mice by reducing JNK-mediated inflammatory responses, suggesting that Rg5 is an effective therapy for hypertensive heart failure.

Peripartum cardiomyopathy

Peripartum cardiomyopathy is cardiovascular disorder that is seen only in females in third trimester to 6 months post delivery. It is a diagnosis of exclusion. The syndrome is still seen in Nigeria more especially Northern Nigeria where the largest cohort of patients were described in the early 70s. The longest follow up (30-35) years of the syndrome was also done in Zaria, Northern Nigeria. The etiology of the syndrome is unknown but from different parts of the world clinicians have associated the syndrome to different risk factors. The authors did a Medline, AJOL and other search to review write ups on this syndrome. Of the 27 publications on the syndrome from Nigeria, 90% came from the Northern Nigeria. In Nigeria the syndrome was associated with the famous Wakan Jeko which composes of a triad of hot baths, ingestion of pap (kunun kanwa) which is made with lake salt that has high levels of sodium (Na + ). Other authors have associated it with hypertension, myocarditis, use of tocolytics and deficiency of trace elements like selenium. Recently the South Africans have also proposed the possibility by products of stress on Prolactin leading to cardiac damage/Peripartum cardiomyopathy has maternal and child health implications in Nigeria, sometimes it does lead to maternal mortality so also infant mortality. Patients have been reported to have developed recurrent Peripartum cardiac failure if they did not take heed to the advice regarding avoiding the wakan jeko. Some of these patients have gone on to develop hypertension and presented with hypertensive cardiac failure or cerebrovascular accident. Peripartum cardiomyopathy etiology is still an enigma. A coordinated national and international effort is required to do a comprehensive research on this syndrome to put to rest or uphold some of the theories regarding etiology.

Acute Cardiac Failure in a Pregnant Woman due to Thyrotoxic Crisis.

Introduction. Cardiac failure during pregnancy is usually related to preeclampsia/eclampsia, rarely to hyperthyroidism. While hyperthyroidism can easily lead to hypertensive cardiac failure and may harm the fetus, it is sometimes difficult to distinguish hyperthyroidism from normal pregnancy. Case Presentation. We encountered a case of 41-year-old pregnant woman with hypertensive cardiac failure. Because we initially diagnosed as pre-eclampsia/eclampsia, Caesarian section was performed. However, her symptoms still persisted after delivery. After thyroid function test results taken on the day of admission were obtained on the fourth day, we could diagnose that her cardiac failure was caused by thyrotoxic crisis. Conclusions. Hypertensive cardiac failure due to hyperthyroidism during pregnancy is rare and difficult to diagnose because of similar presentation of normal pregnancy. However, physicians should be aware of the risks posed by hyperthyroidism during pregnancy.

Anesthésie pour traitement des tumeurs endocrines

Endocrine tumors could be defined by their ability to produce structural proteins or hormones common to nervous and endocrine cells. They might induce physiological transforms or outcome adverse events which should be well known in order to prevent or treat them early. The goal of this review was to describe these changes, to describe preoperative assessment, and to discuss intraoperative monitoring and drugs choice based on the literature from the last 30 years. As an example, it should be noticed that: (1) preoperative blood pressure control is essential to prepare phaeochromocytoma for surgery. It should be followed during anaesthesia by intensive fluid load, reversible anaesthetic drugs and rational cardiovascular medications use (as for example remifentanil, sevoflurane, calcium channel blockers and esmolol), and after surgery by narrow clinical and biological monitoring; (2) after medullar thyroid cancer, main adverse events include cervical compressive haematoma and recurrent laryngeal nerve injury as for any thyroid surgery; (3) during pituitary surgery, air embolism might be expected, whereas water dysregulation (diabetes insipidus), corticotroph insufficiency, cerebrospinal fluid (CSF) leak might occur postoperatively. In acromegaly, difficult endotracheal intubation is possible whereas severe Cushing's syndrome may be complicated with hypertensive cardiac failure, infections, thrombosis, delayed cicatrisation; (4) somatostatine analogs are a keystone in carcinoid tumors preoperative and anaesthetic management.

Recent Advances in Breast Cancer-Related Lymphedema of the Arm: Lymphatic Pump Failure and Predisposing Factors

Axillary surgery for breast cancer may be followed, months to years later, by chronic arm lymphedema. A simple 'stopcock' mechanism (reduced lymph drainage from the entire limb through surviving lymphatics) does not explain many clinical aspects, including the delayed onset and selective sparing of some regions, e.g., hand. Quantitative lymphoscintigraphy reveals that lymph drainage is slowed in the subcutis, where most of the edema lies, and in the subfascial muscle compartment, which normally has much higher lymph flows than the subcutis. Although the muscle does not swell significantly, the impaired muscle drainage correlates with the severity of arm swelling, indicating a likely key role for muscle lymphatic function. A new method, lymphatic congestion lymphoscintigraphy, showed that the edema is associated with a reduced contractility of the arm lymphatics; the weaker the active lymphatic pump, the greater the swelling. Delayed lymphatic pump failure may result from chronic raised afterload, as in hypertensive cardiac failure, and may account for the delayed onset of swelling. A further novel finding is that lymph flow is raised in both the subcutis and muscle of both arms in postsurgical breast patients who later developed breast cancer-related lymphedema (BCRL), compared with patients who did not develop BCRL. This new observation indicates a predisposition to BCRL in some women. Further evidence for predisposing abnormalities is the finding of lymphatic abnormalities in the contralateral (nonswollen) arm in women with established BCRL. Such predisposing factors could explain why some women develop BCRL after sentinel node biopsy, whereas others do not after clearance surgery. Future research must focus on prospective observations made from before surgery until BCRL develops.

Human lymphatic pumping measured in healthy and lymphoedematous arms by lymphatic congestion lymphoscintigraphy

Axillary surgery for breast cancer partially obstructs lymph outflow from the arm, chronically raising the lymphatic smooth muscle afterload. This may lead to pump failure, as in hypertensive cardiac failure, and could explain features of breast cancer treatment-related lymphoedema (BCRL) such as its delayed onset. A new method was developed to measure human lymphatic contractility non-invasively and test the hypothesis of contractile impairment. 99mTc-human IgG (Tc-HIG), injected into the hand dermis, drained into the arm lymphatic system which was imaged using a gamma-camera. Lymph transit time from hand to axilla, ttransit, was 9.6+/-7.2 min (mean+/-s.d.) (velocity 8.9 cm min(-1)) in seven normal subjects. To assess lymphatic contractility, a sphygmomanometer cuff around the upper arm was inflated to 60 mmHg (Pcuff) before 99mTc-HIG injection and maintained for>>ttransit. When Pcuff exceeded the maximum pressure generated by the lymphatic pump (Ppump), radiolabelled lymph was held up at the distal cuff border. Pcuff was then lowered in 10 mmHg steps until 99mTc-HIG began to flow under the cuff to the axilla, indicating Ppump>or=Pcuff. In 16 normal subjects Ppump was 39+/-14 mmHg. Ppump was 38% lower in 16 women with BCRL, namely 24+/-19 mmHg (P=0.014, Student's unpaired t test), and correlated negatively with the degree of swelling (12-56%). Blood radiolabel accumulation proved an unreliable measure of lymphatic pump function. Lymphatic congestion lymphoscintigraphy thus provided a quantitative measure of human lymphatic contractility without surgical cut-down, and the results supported the hypothesis of lymphatic pump failure in BCRL.

Hypertensive Heart Failure Presenting in Labour: A Case Report

Peripartum heart disease is worldwide in distribution but appears most commonly in multiparous black women with a low socio-economic background1. Hypertensive disorders associated with pregnancy can be classified into three groups: Chronic, transient and pre?eclamptic hypertension2. Whereas chronic and transient hypertension do not affect the outcome of pregnancy appreciably, pre-eclampsia presents a potential danger to the mother and fetus. Cardiac failure among pregnant northern Nigerian Women has been reported to occur more frequently in the postnatal period3. Hypertensive cardiac failure has been seen in pregnant women in our practice, but none was seen in association with labour. In a series, only 1.13% of the women with heart disease developed heart failure during labour 4. We report a fatal case of hypertensive heart failure in labour from our centre. Key Words: Hypertensive Heart Failure, Labour Journal of College of Medicine Vol.9(1) 2004: 34-35

Cardiovascular disease in patients on chronic hemodialytic therapy

D URING the early 1970s it became apparent that patients maintained on chronic hemodialysis programs died of cardiovascular disease with an incidence greatly in excess of the age-adjusted expected rate. As a larger number of patients with diabetes, severe hypertension, and preexisting heart disease have become candidates for chronic hemodialysis, elucidation of the exact causes of and factors contributing to the development and progression of cardiovascular disease in end-stage renal failure has become an issue of practical significance. Several earlier reviews of mortality in highly selected, “better risk” dialysis patients reveal an extremely high incidence of cardiovascular complications.‘*2 Lindner et a1.2 reported a sharp increase in the cause-specific mortality from cardiac problems beginning 4 yr after the institution of hemodialysis. Included in this report were three patients with intractable congestive heart failure, as well as eight with myocardial infarction and three patients with stroke. When considered as a single risk factor, the death rate from myocardial infarction rose steeply after 6 yr. A comparison of these data with the incidence of coronary artery disease in the Framingham study3 demonstrates that young dialysis patients have a mortality 2.5 times that reported for older men with severe levels of hypertension.4 Data collected from European centers indicate a similar pattern.’ Among 12,000 deaths occurring in patients on chronic dialysis programs through 1976, 58% were due to cardiovascular disease. Of these, almost half were attributed to “hypertensive cardiac failure,” cardiac arrest, and “other causes of cardiac failure.” Lazarus et a1.,4 after reviewing these data, data from the U.S. National Registry, and data from their own series, concluded that “hemodialysis patients are dying from complications of vascular disease. ” “Accelerated atherosclerosis” was the term used by Lindner et al.* to characterize this unexpected increase in cardiovascular deaths. Although several physical and metabolic abnormalities associated with cardiovascular disease can be shown to be prevalent in the hemodialysis population, there is no direct evidence that these abnormalities can either cause or accelerate atherosclerosis in this patient group. Indeed, a more recent study by Burke et al.’ indicates that patients who do not have diabetes, underlying heart disease, or malignant hypertension before entering dialysis programs have a very low incidence of subsequent atherosclerotic complications. None of the 24 deaths in this group was due to cardiac disease, although 7 deaths occurred after more than 5 yr on dialysis. Almost half of the deaths Burke et al. reported were due to infection, while small numbers were due to dialysis dementia, hyperkalemia, voluntary discontinuance, and miscellaneous other causes. In contrast, 8 of 10 deaths occurring after more than 5 yr of dialysis in Lindner’s group were due directly to cardiac disease, and 7 of these were “coronary deaths.“* Burke et al.* suggested that the discordant experiences may be due to a fundamental change in the physical composition of the dialysis population. They point out that case selection greatly influences the conclusions drawn from these retrospective studies, since the incidence of myocardial infarction and stroke was 34% in a group of patients excluded from their analysis (Table 1). In order to estimate the contribution of chronic hemodialysis to cardiovascular disease, it is necessary to evaluate the cardiac status of patients before entry into dialysis programs. Studies of cardiac function have the disadvantage that day-to-day alterations in diet, fluid balance, or compliance with medical therapy may be responsible for large fluctuations in a

Apresoline intolerance with bladder paralysis.

A CASE of bladder paralysis in a fifty-eight-year-old woman who was taking Apresoline (1-hydrazinophthalazine hydrochloride) was recently reported by Goldstein et al.‡ The patient had had a surgical operation involving the bladder, and although there was no apparent connection between the operation and the paralysis, it seems desirable to present another case to help establish whether the disturbance was actually due to Apresoline.Case ReportA 68-year-old woman was admitted to the hospital suffering from mild hypertensive cardiac failure. During a week's rest in bed the average blood pressure was 220/90, and it was decided to treat her with Apresoline . . .