Protective effect of pulmonary hypertension against right-sided tamponade in pericardial effusion.

Patients with pericardial effusion are susceptible to cardiac tamponade. A compressing circumferential pericardial effusion typically results in an equalization of intracardiac and pericardial pressure during diastole and a progressive collapse of the right atrium and ventricle. Pulmonary hypertension that increases the afterload of the right ventricle may result in elevated pressures initially in the right ventricle and subsequently in the right atrium. This may lead to right ventricular hypertrophy and a pathologic structural and functional remodeling of both right heart chambers. Conversely, elevated pressures within the right heart chambers caused by longstanding pulmonary hypertension may resist and protect against tamponade of these chambers in the setting of a coexisting pericardial effusion. In such cases, a sudden reduction in pulmonary arterial pressures may result in tamponade of the right heart chambers.

Nebivolol: a multifaceted antioxidant and cardioprotectant in hypertensive heart disease.

Cardiomyocyte necrosis with attendant microscopic scarring is a pathological feature of human hypertensive heart disease (HHD). Understanding the pathophysiological origins of necrosis is integral to its prevention. In a rat model of HHD associated with aldosterone/salt treatment (ALDOST), myocyte necrosis is attributable to oxidative stress induced by cytosolic-free [Ca]i and mitochondrial [Ca]m overloading in which the rate of reactive oxygen species generation overwhelms their rate of detoxification by endogenous Zn-based antioxidant defenses. We hypothesized that nebivolol (Neb), unlike another ß1 adrenergic receptor antagonist atenolol (Aten), would have a multifaceted antioxidant potential based on its dual property as a ß3 receptor agonist, which activates endothelial nitric oxide synthase to stimulate nitric oxide (NO) generation. NO promotes the release of cytosolic Zn sequestered inactive by its binding protein, metallothionein. Given the reciprocal regulation between these cations, increased [Zn]i reduces Ca entry and attendant rise in [Ca]i and [Ca]m. Herein, we examined the antioxidant and cardioprotectant properties of Neb and Aten in rats receiving 4 weeks ALDOST. Compared with untreated age-/sex-matched controls, ALDOST alone or ALDOST with Aten, Neb cotreatment induced endothelial nitric oxide synthase activation, NO generation and a marked increase in [Zn]i with associated decline in [Ca]i and [Ca]m. Attendant antioxidant profile at subcellular and cellular levels included attenuation of mitochondrial H2O2 production and lipid peroxidation expressed as reduced 8-isoprostane concentrations in both mitochondria and cardiac tissue. Myocyte salvage was expressed as reduced microscopic scarring and tissue collagen volume fraction. Neb is a multifaceted antioxidant with unique properties as cardioprotectant in HHD.

Mitochondria play a central role in nonischemic cardiomyocyte necrosis: common to acute and chronic stressor states.

The survival of cardiomyocytes must be ensured as the myocardium adjusts to a myriad of competing physiological and pathophysiological demands. A significant loss of these contractile cells, together with their replacement by stiff fibrillar collagen in the form of fibrous tissue accounts for a transition from a usually efficient muscular pump into one that is failing. Cellular and subcellular mechanisms involved in the pathogenic origins of cardiomyocyte cell death have long been of interest. This includes programmed molecular pathways to either necrosis or apoptosis, which are initiated from ischemic or nonischemic origins. Herein, we focus on the central role played by a mitochondriocentric signal-transducer-effector pathway to nonischemic cardiomyocyte necrosis, which is common to acute and chronic stressor states. We begin by building upon the hypothesis advanced by Albrecht Fleckenstein and coworkers some 40 years ago based on the importance of calcitropic hormone-mediated intracellular Ca(2+) overloading, which predominantly involves subsarcolemmal mitochondria and is the signal to pathway activation. Other pathway components, which came to be recognized in subsequent years, include the induction of oxidative stress and opening of the mitochondrial inner membrane permeability transition pore. The ensuing loss of cardiomyocytes and consequent replacement fibrosis, or scarring, represents a disease of adaptation and a classic example of when homeostasis begets dyshomeostasis.

Reverse remodeling and recovery from cachexia in rats with aldosteronism.

The congestive heart failure (CHF) syndrome with soft tissue wasting, or cachexia, has its pathophysiologic origins rooted in neurohormonal activation. Mechanical cardiocirculatory assistance reveals the potential for reverse remodeling and recovery from CHF, which has been attributed to device-based hemodynamic unloading whereas the influence of hormonal withdrawal remains uncertain. This study addresses the signaling pathways induced by chronic aldosteronism in normal heart and skeletal muscle at organ, cellular/subcellular, and molecular levels, together with their potential for recovery (Recov) after its withdrawal. Eight-week-old male Sprague-Dawley rats were examined at 4 wk of aldosterone/salt treatment (ALDOST) and following 4-wk Recov. Compared with untreated, age-/sex-/strain-matched controls, ALDOST was accompanied by 1) a failure to gain weight, reduced muscle mass with atrophy, and a heterogeneity in cardiomyocyte size across the ventricles, including hypertrophy and atrophy at sites of microscopic scarring; 2) increased cardiomyocyte and mitochondrial free Ca(2+), coupled to oxidative stress with increased H(2)O(2) production and 8-isoprostane content, and increased opening potential of the mitochondrial permeability transition pore; 3) differentially expressed genes reflecting proinflammatory myocardial and catabolic muscle phenotypes; and 4) reversal to or toward recovery of these responses with 4-wk Recov. Aldosteronism in rats is accompanied by cachexia and leads to an adverse remodeling of the heart and skeletal muscle at organ, cellular/subcellular, and molecular levels. However, evidence presented herein implicates that these tissues retain their inherent potential for recovery after complete hormone withdrawal.

Microscopic abnormality classification of cardiac murmurs using ANFIS and HMM.

Auscultation of heart dispenses identification of the cardiac valves. An electronic stethoscope is used for the acquisition of heart murmurs that is further classified into normal or abnormal murmurs. The process of heart sound segmentation involves discrete wavelet transform to obtain individual components of the heart signal and its separation into systole and diastole intervals. This research presents a novel scheme to develop a semi-automatic cardiac valve disorder diagnosis system. Accordingly, features are extracted using wavelet transform and spectral analysis of input signals. The proposed classification scheme is the fusion of adaptive-neuro fuzzy inference system (ANFIS) and HMM. Both classifiers are trained using the extracted features to correctly identify normal and abnormal heart murmurs. Experimental results thus achieved exhibit that proposed system furnishes promising classification accuracy with excellent specificity and sensitivity. However, the proposed system has fewer classification errors, fewer computations, and lower dimensional feature set to build an intelligent system for detection and classification of heart murmurs.

Computer-assisted brain tumor type discrimination using magnetic resonance imaging features.

Medical imaging plays an integral role in the identification, segmentation, and classification of brain tumors. The invention of MRI has opened new horizons for brain-related research. Recently, researchers have shifted their focus towards applying digital image processing techniques to extract, analyze and categorize brain tumors from MRI. Categorization of brain tumors is defined in a hierarchical way moving from major to minor ones. A plethora of work could be seen in literature related to the classification of brain tumors in categories such as benign and malignant. However, there are only a few works reported on the multiclass classification of brain images where each part of the image containing tumor is tagged with major and minor categories. The precise classification is difficult to achieve due to ambiguities in images and overlapping characteristics of different type of tumors. In the current study, a comprehensive review of recent research on brain tumors multiclass classification using MRI is provided. These multiclass classification studies are categorized into two major groups: XX and YY and each group are further divided into three sub-groups. A set of common parameters from the reviewed works is extracted and compared to highlight the merits and demerits of individual works. Based on our analysis, we provide a set of recommendations for researchers and professionals working in the area of brain tumors classification.

K+ and Mg2+ Dyshomeostasis in Acute Hyperadrenergic Stressor States.

Acute stressor states are linked to neurohormonal activation that includes the adrenergic nervous system. Elevations in circulating epinephrine and norepinephrine unmask an interdependency that exists between K+ and Mg2+ based on their regulation of a large number of Mg2+-dependent Na+-K+-ATPase pumps present in skeletal muscle. The hyperadrenergic state accounts for a sudden translocation of cations into muscle with the rapid appearance of hypokalemia and hypomagnesemia. The resultant hypokalemia and hypomagnesemia will cause a delay in myocardial repolarization and electrocardiographic QTc prolongation raising the propensity for supraventricular and ventricular arrhythmias. In this review, we focus on the interdependency between K+ and Mg2+, which is clinically relevant to acute hyperadrenergic stressor states found in patients admitted to intensive care units.

Idiopathic intracranial hypertension associated with either primary or secondary aldosteronism.

BACKGROUND: Idiopathic intracranial hypertension (IIH) is a syndrome consisting of headache, visual field defects and papilledema of uncertain etiology. The prospect was raised previously as to an association between aldosteronism and increased intracranial pressure in 2 middle-aged women with IIH and primary aldosteronism (PAL). Since then, 2 additional adults were identified and 2 other cases were reported from the United Kingdom, whereas 6 cases of IIH and secondary aldosteronism (SAL) in children have been reported in the English literature worldwide. METHODS: A retrospective analysis of cases from author institutions and published literature comparing clinical features, laboratory findings and therapeutic interventions in these 12 cases. RESULTS: The female-to-male ratio was 10:2. The mean age of the PAL patients was 49 ± 3 years-all hypertensive, with adrenal pathology in most. The mean age of the SAL patients was 11 ± 2 years-mostly normotensive, with 3 having Bartter's and 2 Gitelman syndromes, and 1 renal congenital hypoplasia. Plasma aldosterone levels were elevated (31 ± 5 ng/dL) in PAL and SAL, whereas plasma renin activity was suppressed in PAL. Hypokalemia (3.2 ± 0.2 mmol/L), hypomagnesemia (1.6 ± 0.3 mg/dL) and a putative metabolic alkalosis (serum HCO3 30 ± 1 mmol/L) were observed. IIH symptoms were controlled by spironolactone in 5, amiloride in 1, correction of hypokalemia and hypomagnesemia in 2, discontinuation of nonsteroidal anti-inflammatory drugs in 2, and reduction of body weight in 1. One patient required serial lumbar punctures, 2 a ventriculoperitoneal shunt, whereas all 3 patients with adrenal adenoma underwent surgical resection. CONCLUSIONS: An association between IIH and PAL occurs in hypertensive middle-aged women, whereas normotensive girls having an inherited renal tubular defect may have IIH with SAL. Patients with IIH should be evaluated for aldosteronism and considered for spironolactone therapy.

Cation interdependency in acute stressor states.

Acute stressor states are inextricably linked to neurohormonal activation which includes the adrenergic nervous system. Consequent elevations in circulating epinephrine and norepinephrine unmask an interdependency that exists between K+, Mg2+ and Ca2+. Catecholamines, for example, regulate the large number of Mg2+-dependent Na/K ATPase pumps present in skeletal muscle. A hyperadrenergic state accounts for a sudden translocation of K+ into muscle and rapid appearance of hypokalemia. In the myocardium, catecholamines promote Mg2+ efflux from cardiomyocytes, whereas intracellular Ca2+ influx and overloading account for the induction of oxidative stress and necrosis of these cells with leakage of their contents, including troponins. Accordingly, acute stressor states can be accompanied by nonischemic elevations in serum troponins, together with the concordant appearance of hypokalemia, hypomagnesemia and ionized hypocalcemia, causing a delay in myocardial repolarization and electrocardiographic QTc prolongation raising the propensity for arrhythmias, including atrial fibrillation and polymorphic ventricular tachycardia. In this review, we focus on the interdependency between K+, Mg2+ and Ca2+ which are clinically relevant to acute stressor states.

Cardiogenic shock following electro-cardioversion of new onset atrial flutter.

Transient hypotension and atrial stunning are known complications of electro-cardioversion for supra-ventricular tachyarrhythmias, however, a clinically significant cardiac failure is extremely rare in this setting. We, herein, present a 77-year-old African American male who underwent electro-cardioversion following an unremarkable transesophageal echocardiogram (TEE) for a symptomatic atrial flutter of a new onset. Immediately post-cardioversion, he suffered severe hypotension with a depressed LV systolic function. IV dobutamine stabilized his blood pressure.

Nonsustained ventricular tachycardia induced by valsalva manoeuvre in a patient with nonobstructive hypertrophic cardiomyopathy.

Cardiac arrhythmias are rarely inducible in patients with hypertrophic cardiomyopathy on provocative manoeuvres to identify latent obstruction. We present a 40-year-old male with history of nonobstructive hypertrophic cardiomyopathy who presented with lightheadedness. Echocardiogram showed severe asymmetric hypertrophy of the left ventricle without left ventricular outflow tract gradient at rest. On Doppler study with Valsalva manoeuvre, he developed symptomatic nonsustained ventricular tachycardia, which was reproduced on repetition. This emphasizes the importance of provocative manoeuvres to unmask potentially significant physiologic manifestations.

Disturbances in calcium metabolism and cardiomyocyte necrosis: the role of calcitropic hormones.

A synchronized dyshomeostasis of extra- and intracellular Ca(2+), expressed as plasma ionized hypocalcemia and excessive intracellular Ca(2+) accumulation, respectively, represents a common pathophysiologic scenario that accompanies several diverse disorders. These include low-renin and salt-sensitive hypertension, primary aldosteronism and hyperparathyroidism, congestive heart failure, acute and chronic hyperadrenergic stressor states, high dietary Na(+), and low dietary Ca(2+) with hypovitaminosis D. Homeostatic responses are invoked to restore normal extracellular [Ca(2+)](o), including increased plasma levels of parathyroid hormone and 1,25(OH)(2)D(3). However, in cardiomyocytes these calcitropic hormones concurrently promote cytosolic free [Ca(2+)](i) and mitochondrial [Ca(2+)](m) overloading. The latter sets into motion organellar-based oxidative stress, in which the rate of reactive oxygen species generation overwhelms their detoxification by endogenous antioxidant defenses, including those related to intrinsically coupled increments in intracellular Zn(2+). In turn, the opening potential of the mitochondrial permeability transition pore increases, allowing for osmotic swelling and ensuing organellar degeneration. Collectively, these pathophysiologic events represent the major components to a mitochondriocentric signal-transducer-effector pathway to cardiomyocyte necrosis. From necrotic cells, there follows a spillage of intracellular contents, including troponins, and a subsequent wound healing response with reparative fibrosis or scarring. Taken together, the loss of terminally differentiated cardiomyocytes from this postmitotic organ and the ensuing replacement fibrosis each contribute to the adverse structural remodeling of myocardium and progressive nature of heart failure. In conclusion, hormone-induced ionized hypocalcemia and intracellular Ca(2+) overloading comprise a pathophysiologic cascade common to diverse disorders and that initiates a mitochondriocentric pathway to nonischemic cardiomyocyte necrosis.