Canadian Health&Care Mall: The Ballooning Posterior Leaflet Syndrome

cardiac arrhythmiasThe validity scales revealed no abnormalities. Seven of the eight symptom-free patients had entirely normal MMPIs. The eighth, discovered because she was the niece of a woman who died from the ballooning posterior leaflet syndrome, showed an abnormal test score for hypomania. Of the six symptomatic patients with the full ballooning posterior leaflet syndrome (Table 1), five had abnormal scores for hysteria and hypochondriasis, four showed abnormal scores for depression, psychopathic deviate and schizophrenia, three had abnormal scores for psychasthenia, two had abnormal scores for social inversion, and one showed abnormal scores for paranoia, hypomania and masculinity-femininity. All these symthoms can be abserved at patients suffering from “persecution syndrome”. Canadian Health&Care Mall has all the necessary medicaments and qualified stuff to held you deal with the treatment of such disorders – Two of these six patients have been resuscitated from a near-fatal arrhythmia (patients 2 and 6), and two have demonstrated frequent PVCs during electrocardiographic monitoring procedures (patients 4 and 5). The two patients with life-threatening arrhythmias (ventricular fibrillation and ventricular tachycardia) were abnormal in at least four categories of the MMPI, while the other patients showed abnormal elevations on at least three of the scales.

Of the four patients with valvular aortic stenosis, all presented with angina pectoris, two with exertional shortness of breath, and one with occasional dizziness. All four exhibited normal MMPIs with normal validity scales (Table 2). Continue reading “Canadian Health&Care Mall: The Ballooning Posterior Leaflet Syndrome”


The Ballooning Posterior Leaflet Syndrome: Minnesota Multiphasic Personality Inventory Profiles in Symptomatic and Asymptomatic Groups

vague symptomsIn the process of evaluating an increasing number of people presenting with a midsystolic click and/or late systolic murmur, it became apparent that two distinct groups could be identified: Group 1 consists of patients who were referred for some other reason, are totally asymptomatic, have a mid-systolic click and/or a late systolic murmur on auscultation, and exhibit a typical ballooning posterior leaflet on echocardiography not due to any demonstrable organic heart disease. This group appears to be quite common. A second group of patients, presenting not only with the midsystolic click and/or late systolic murmur and a positive echocardiogram for ballooning posterior leaflet but also with overt symptomatology, are considered to have the ballooning posterior leaflet syndrome.

The inordinate emotional lability and many vague symptoms (chest pain, fatigue, palpitations) in patients with the complete syndrome was impressive. Indeed, symptoms of “neuropsychiatric origin” appeared to play a role in many of those patients described by Hancock and Jeresaty. In addition, the observation that emotional lability contributed to the sudden death of two patients with the ballooning posterior leaflet syndrome raised the question as to whether objective assessment of personality features might help to identify patients with the full syndrome particularly at risk for sudden death. A standardized personality test, the Minnesota Multiphasic Personality Inventory (MMPI), was, therefore, given to both groups of patients in an effort to more objectively assess the presence of gross psychopathology. Continue reading “The Ballooning Posterior Leaflet Syndrome: Minnesota Multiphasic Personality Inventory Profiles in Symptomatic and Asymptomatic Groups”

Canadian Health&Care Mall: Congenital Heart Disease in a Tetra-X Woman

congenital heart diseaseTetra-X is a rare abnormality of the sex chromosomes; only 20 cases have been reported previously. It is thought to result from nondisjunctions during the first and second meiotic divisions of oogenesis. The clinical features are nonspecific and have included mental retardation reduction of dermal ridges, behavioral disturbances, hypertelorism with epicanthal folds, eye anomalies (myopia, squints, nystagmus, iridoschisis), skeletal abnormalities (clinodactyly, radioulnar synostosis, dislocation of the hip, tall stature), menstrual irregularities with reduced fertility, and congenital heart disease.

The patient to be presented is the first case of tetra-X to be studied at autopsy and the first with documented congenital heart disease. Read more about congenital heart disease on Canadian Health&care Mall – Continue reading “Canadian Health&Care Mall: Congenital Heart Disease in a Tetra-X Woman”

Erectile Dysfunction: Treatment & Care

EDCauses of Erectile Dysfunction (ED)

Often abbreviated as ED, erectile dysfunction is a consistent or reoccurring inability to obtain or maintain an erection satisfactory for sexual performance. It affects an estimated 30 million men in the United States. Erectile dysfunction is occurs frequently in men with diabetes, high blood pressure, high cholesterol, heart disease, vascular disease, neurological diseases and other major illnesses and disorders.

Psychological factors include stress, anxiety, depression and relationship problems. Lifestyle risk factors include obesity, lack of physical activity, smoking and excessive alcohol consumption. Other contributing factors include various prescribed medications. Studies have shown that men who suffer from erectile dysfunction were twice as likely to have diabetes as compared to healthy, unaffected men.

Erectile Dysfunction (ED) and Other Health Risks

Research has shown recently that erectile dysfunction can be an early warning symptom of important diabetes and cardiovascular problems. Erectile dysfunction predicts and precedes the metabolic syndrome several years in advances. Similarly erectile dysfunction predicts and precedes a heart attack 3 years in advance. Such new information affords a great warning for middle aged men to go to the doctor and get the appropriate evaluation. Furthermore, sexual health becomes the portal to men’s health motivating men to pursue healthy lifestyle such as weight control, physical exercise, quitting smoking and controlling alcohol.

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Canadian Health&Care Mall: RV Resuscitation of Pulmonary Embolism in the Critically III

 RV functionWhen PE impairs RV function, further possible consequences include low cardiac output and shock and myocardial ischemia due to poor coronary perfusion pressure and diastolic overdistension. Enlarged right-sided chambers can push the septae into left-sided chambers, limiting their diastolic filling and interfering with systolic contractile function. While each PE patient’s heart is different due to a different preexisting extent of cardiopulmonary disease, some practices have evolved reflecting sensible physiologically based management.

Volume Administration

The use of judicious volume infusion in resuscitating the RV has been shown to improve cardiac output in PE patients with decreased RV preload. While provision of adequate RV preload is essential for cardiac output, overdistension of the RV with volume resuscitation can impair coronary perfusion and LV filling, diminishing LV output. In a report of a small series of patients with acute PE and a cardiac index < 2.5 L/min/m2, treatment with 500 mL of dextran significantly increased cardiac index from a mean of 1.6 to 2.0 L/min/m2. Continuous cardiac output pulmonary artery catheters allowed the calculation of RV end-diastolic index; patients with low values had a greater improvement with fluid therapy offered by Canadian Health&Care Mall. Currently, an author of that report (A. Mercat, MD; personal communication; June 2006) uses echocardiography in underperfusing PE patients to guide fluid crystalloid infusion until the RV:LV diastolic diameter ratio appears to be 1.0. The RV is then considered adequately filled, and IV dobutamine and norepinephrine are added as needed. “Prophylactic” early intubation with positive pressure ventilation is avoided because of its potential interference with RV preload.

Continue reading “Canadian Health&Care Mall: RV Resuscitation of Pulmonary Embolism in the Critically III”

Pneumococcal Adherence to the Buccal Epithelial Cells of Cigarette Smokers: Results and Disscusion

smokersBackground adherence values were not significantly different in smokers (9.1 ±9.1), exsmokers (4.8±6.4), and nonsmokers (8.5±21.1). However, after incubation with S pneumoniae type 25, the pneumococcal adherence to ВЕС of smokers (12.3 ±6.9) was significantly greater (p<0.001) than that of nonsmokers (0.7±0.4), as shown in Figure 1. There was poor correlation between background adherence and pneumococcal adherence in nonsmokers (r = 0.5) and smokers (r=0.68). Smokers’ and nonsmokers’ ВЕС were indistinguishable in terms of maturation as determined microscopically. The correlation coefficient for the blinded adherence estimates between the two readers was.95,.90 and.85 for S, ES, and NS, respectively.

The reproducibility of the elevated pneumococcal adherence estimates is shown in Table 1. The mean pneumococcal adherence for the repeat adherence measurements is not significantly different from the original value, and the reproducibility for each individual subject also appears to be good.

There is no predictable relationship between either smokers age (r = 0.01) or pack years of smoking (r = 0.03) to pneumococcal adherence. Three years after cessation of smoking, all subjects have adherence values (0.5 ±0.4) which fall in the range of the nonsmokers, as shown in Figure 2. Prior to the three years, six of 13 had elevated values but the degree of elevation in these six (4.5 ±2.1) is significantly (p<0.05) less than that of current smokers (12.3 ±6.9). All exsmokers with elevated adherence had serum thiocyanate levels which were within the normal range. No pneumococci were isolated from any smoking or nonsmoking subjects.

The effect of smokers’ saliva on pneumococcal adherence to ВЕС of nonsmokers is shown in Table 2. Pneumococcal adherence to ВЕС of nonsmokers is similar when the cells are incubated with either the nonsmokers own saliva (1.1 ±0.9) or with saliva of another nonsmoker (0.9 ±0.2) but is significantly increased (p<0.001) to 8.2 ±4.4 by incubation of these cells in smokers saliva. The pneumococcal adherence to ВЕС of smokers, on the other hand, is not significantly changed by incubating their cells in their own saliva or in nonsmokers saliva (21.0± 13.8 to 16.2 ±6.2).

The salivary amylase in smokers was elevated compared to nonsmokers (135,800 vs 69,300 m|x/ml) and the SGOT of smokers was lower (10 vs 27 mp7ml). mucosal surface


Bacterial adherence to cells is tissue- as well as host-specific and it is an essentially irreversible molecular interaction between cell surfaces. It is believed to determine the ability of bacteria to colonize and to perhaps infect and invade many mucosal surfaces.

Several studies have shown a relationship between increased bacterial adherence to buccal or pharyngeal mucosal cells and the development of pneumonia. Johanson et al have shown that increased in-vitro adherence of Pseudomonas aeruginosa, Klebsiella pneumoniae, E coli, and Proteus mirabilis to buccal epithelial cells is associated with in-vivo colonization, which in turn has been correlated with increased risk of nosocomial pneumonia. Influenza infection has been shown to increase the adherence of Staphylococcus aureus, S pneumoniae, and Hemophilus influenza to pharyngeal epithelial cells. These organisms cause pneumonias which complicate influenzal respiratory illness.

This finding of increased adherence of type 25 S pneumoniae to smokers’ buccal epithelial cells is similar to the increased adherence demonstrated by Fainstein and Musher for type 1 and type 3 S pneumoniae. In both studies, there was no difference in background adherence values between smokers and nonsmokers. Ibis suggests that the increased adherence in smokers is mediated by some specific mechanism rather than a generalized increase in avidity of bacteria for smokers’ buccal epithelial cells. Pneumococcal adherence in smokers remained constantly elevated over a 14-week interval. Thus, day-to-day variations in cigarette consumption, oral hygiene, or other acute effects of cigarette smoking are probably not important factors in detemining adherence of S pneumoniae to buccal epithelial cells.

Adherence does not vary with age or duration of smoking. That is, it appears that pneumococcal adherence in smokers is fully expressed after a few years of smoking and does not intensify thereafter. Therefore, if adverse clinical consequences accrue from an increased adherence of Pneumococcus to oral epithelial cells, young smokers are at risk early in their smoking history. In this regard, the increased incidence of pneumonia in adolescent and young adult cigarette smokers is of interest.

The persistent adherence in exsmokers might be due to continued smoking, but the observation that these subjects had serum thiocyanate levels (half-life of 14 days) within the nonsmokers’ range gives us confidence that the history of smoking cessation given by these nonpaid volunteers was correct.

Using routine clinical laboratory techniques, none of our subjects had positive pharyngeal cultures for S pneumoniae. Similarly, the enhanced in-vitro adherence of S pneumoniae following experimentally-induced influenza infection was not associated with pneumococcal colonization. This inability to culture S pneumoniae in asymptomatic cigarette smokers may be in part due to technical difficulties in identifying small numbers of colonized organisms. pneumoniae In any event, these observations do not refute the relation of adherence to colonization, but rather emphasize the multifactorial nature of the interaction of bacteria with their environment. Local defense mechanisms such as bacterial antagonism, surface immunoglobulins, salivary flow, surface fluids chemistry, and cell desquamation exist in the upper airway in-vivo and provide protection against surface colonization. If these are unfavorably altered in the host, the tendency for increased pneumococcal adherence may manifest itself in colonization and subsequent disease may then take place.

The mechanism by which smoking raises adherence and by which the increased adherence was maintained after smoking cessation in some subjects is not known. Hie elevation of nonsmokers adherence after incubation of their epithelial cells in a cell-free filtrate of smoker s saliva suggests that a constituent of smokers saliva alters the surface properties of buccal epithelial cells in a manner that enhances their avidity for Pneumococcus, perhaps by making binding sites on buccal epithelial cells available to type 25 S pneumoniae. Although this study was not designed to determine how this takes place, one possibility is the removal of an antiadherence factor from the epithelial cell. Such a mechanism exists in the urinary tract where adherence of Gram-negative organisms to bladder mucosal cells rises when surface glycosaminogly-cans are removed, and in the oral cavity where removal of fibronectin by trypsin enhances the adherence of Pseudomonas aeruginosa to the buccal cells. Whole saliva contains many enzymes including amylase and trypsin, which may act upon cell surfaces in an analogous fashion to increase pneumococcal adherence. Salivary amylase was elevated in the three of the smoking subjects tested.

It has been shown that in-vitro adherence of S pneumoniae to buccal epithelial cells of cigarette smokers is increased. This increased adherence remains constant over a period of several months in active cigarette smokers and may persist for up to three years after smoking cessation. Since increased adherence of other bacteria to surface cells is an established pathogenetic step in infection in both the lung and other organs, this observation may explain the increased risk of lower respiratory infection that exists in cigarette smokers.’’ This increased adherence is mediated by a factor found in the cell-free filtrate of smokers saliva.


Figure 1. Pneumococcal adherence of 15 nonsmokers and 15 smokers.


Figure 2. Pneumococcal adherence after smoking cessation in 21 exsmokers. Stippled area is the range of normal for smokers.

Table 1—Repeat Measurements of Pneumococcal Adherence in Smokers and Nonsmokers

OCTSmokers JAN
25.1 16.1
5.9 9.2
11.7 16.9
16.0 18.0
12.0 14.0
MEAN ± SD 14.1 ±7.1 14.8±3.5
0.4 0.1
0.2 0.6
1.2 1.7
0.4 0.6
0.4 0.5
0.6 0.3
MEAN ± SD 0.5 ±0.4 0.6±0.6

Table 2—Effect of Incubating Nonsmokers Cells with Own, Other ‘Nonsmokers у and Smokers Saliva

PneumiOwn xx>ccal Adherence (Bact< Other Nonsmokers jria/Cell)Smokers
0.4 0.9 13.3
2.7 0.5 8.6
1.0 0.8 5.5
0.4 1.0 13.5
0.6 0.9 4.4
1.5 1.2 3.8
MEAN±SD 1.1±0.9 0.9±0.2 8.2±4.4

Canadian Health&Care Mall: Research of Pneumococcal Adherence to the Buccal Epithelial Cells of Cigarette Smokers

bacterial colonizationAdherence to certain mucosal surfaces, a prerequisite for bacterial colonization, is believed to be a necessary initiating event in the pathogenesis of human diseases such as endocarditis, cystitis, pyelonephritis, gonococcal urethritis, Gram-negative bacterial pneumonia, shigellosis, and Escherichia coli enteritis. Treat all the mentioned above diseases including cystitis with Canadian Health&Care Mall –

Streptococcus pneumoniae is a common pathogen in cigarette smokers. To examine the relationship between cigarette smoking and adherence of S pneumoniae to buccal epithelial cells, the adherence of type 25 S pneumoniae was measured in smokers, nonsmokers and exsmokers. Findings were related to subject age, duration and intensity of smoking, and period of time after smoking cessation. Also investigated was the effect of saliva, a natural chemical and mechanical barrier, on pneumococcal adherence to these cells. Continue reading “Canadian Health&Care Mall: Research of Pneumococcal Adherence to the Buccal Epithelial Cells of Cigarette Smokers”

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