Mitral valve prolapse syndrome: The effect of adrenergic stimulation

Previous studies demonstrating increased adrenergic tone in symptomatic patients with mitral valve prolapse prompted a study of the response of symptomatic patients with mitral valve prolapse to adrenergic stimulation. Sixteen such patients had plasma catecholamines and 24 hour urinary epinephrine plus norepinephrine values that were greater than those of control subjects (473.3 ± 92.8 pg/ml versus 292 ± 15 and 44.7 ± 2.3 μg/g creatinine versus 29.8 ± 2.3; p < 0.01 and < 0.001, respectively). Twenty-four hour urinary sodium was lower in the patient group than in the control group (75 ± 7.4 versus 141 ±11 mEq; p < 0.01), with an inverse relation between urinary sodium and norephinephrine in the patient group (r = - 0.78) but not in the control group.Isoproterenol infusions, 0.5, 1.0 and 2.0 μg/min for 6 minutes, produced a dose-related, greater increase in heart rate in the mitral valve prolapse group than in the control group (16.1 ± 2.3 versus 10 ± 2; 31.8 ± 3.5 versus 19.6 ± 3; 48 ± 4.1 versus 27 ± 3; p< 0.01 with 0.5, 1.0 and 2.0 μg, respectively). The greater increase in heart rate resulted in a significantly shorter diastolic time in the patient group than in the control group (26.4 ± 2 s/min versus 30.6 ± 2; 27 ± 1.5 versus 30.6 ± 2; 26.6 ± 2 versus 30.9 ± 2; p < 0.01 with 0.5, 1.0 and 2.0 μg, respectively). The QT interval was 25 ms shorter than electromechanical systole (QS2) in the normal group and 26.5 ms shorter than QS2in the mitral valve prolapse group at rest; during isoproterenol infusion QT-QS2values were different in the mitral valve prolapse and control groups (3.3 ± 3 versus -7.0 ± 3; 31.9 ± 2.8 versus 10 ± 4; 52 ± 9.2 versus 29 ± 8; p < 0.01 with 0.5, 1.0 and 2.0 μg/min, respectively). Isoproterenol infusion also reproduced symptoms on a dose-related basis in 14 patients with mitral valve prolapse but not in control subjects (excluding palpitation).Symptomatic patients with mitral valve prolapse and high rest values of catecholamines were hypersensitive to isoproterenol infusion, suggesting that some of the symptoms are catecholamine-related or mediated

The marfan syndrome: Abnormal aortic elastic properties

Aortic distensibility and aortic stiffness index were measured at the ascending aorta (3 cm above the aortic valve) and the mid-portion of the abdominal aorta from the changes in echocardiographic diameters and pulse pressure in 14 patients with the Marfan syndrome and 15 age- and gender-matched normal control subjects. The following formulas were used: 1) Aortic distensibility = 2(Changes in aortic diameter)/(Diastolic aortic diameter) (Pulse pressure); and 2) Aortic stiffness index = ln(Systolic blood pressure)/(Diastolic blood pressure)(Changes in aortic diameter)/Diastolic aortic diameter. Pulse wave velocity was also measured.Compared with normal subjects, patients with the Marfan syndrome had decreased aortic distensibility in the ascending and the abdominal aorta (2.9 ± 1.3 vs. 5.6 ± 1.4 cm2 dynes-1, p < 0.001 and 4.5 ± 2.1, vs. 7.7 ± 2.5, cm2 dynes-1, p < 0.001, respectively) and had an increased aortic stiffness index in the ascending and the abdominal aorta (10.9 ± 5.6 vs. 5.9 ± 2.2, p < 0.005 and 7.1 ± 3.1 vs. 3.9 ± 1.2, p < 0.005, respectively). Aortic diameters in the ascending aorta were larger in these patients than in normal subjects, but those in the abdominal aorta were similar in the two groups. Linear correlations for both aortic distensibility and stiffness index were found between the ascending and the abdominal aorta (r = 0.85 and 0.71, respectively). Pulse wave velocity was more rapid in the patients than in the normal subjects (11.6 ± 2.5 vs. 9.5 ± 1.4 m/s, respectively, p < 0.01).Thus, aortic elastic properties are abnormal in patients with the Marfan syndrome irrespective of the aortic diameter, which suggests an intrinsic abnormality of the aortic arterial wall

Floppy mitral valve/mitral valve prolapse syndrome: Beta-adrenergic receptor polymorphism may contribute to the pathogenesis of symptoms

AbstractBackgroundCertain patients with floppy mitral valve (FMV)/mitral valve prolapse (MVP) may have symptoms that cannot be explained on the severity of mitral valvular regurgitation (MVR) alone; hypersensitivity to adrenergic stimulation has been suggested in this group defined as the FMV/MVP syndrome.MethodsNinety-eight patients (75 men, 23 women) with mitral valve surgery for FMV/MVP were studied. Of those 41 (42%) had symptoms consistent with FMV/MVP syndrome [29 men (39%), 12 women (52%)]; median age of symptom onset was 30 years (range 10–63 years) and median duration of symptoms prior to valve surgery was 16 years (range 3–50 years). Ninety-nine individuals (70 men, 29 women) without clinical evidence of any disease were used as controls. Genotyping of β1 and β2 adrenergic receptors was performed.Resultsβ-Adrenergic receptor genotypes (β1 and β2) were similar between control and overall FMV/MVP patients. Subgroup analysis of patients, however, demonstrated that the genotype C/C at position 1165 resulting in 389 Arg/Arg of the β1 receptor was more frequent in women compared to those without FMV/MVP syndrome and to normal control women (p<0.025). This polymorphism may be related to hypersensitivity to adrenergic stimulation as reported previously in these patients.ConclusionThis study shows a large proportion of patients with FMV/MVP, predominantly women, had symptoms consistent with the FMV/MVP syndrome for many years prior to the development of significant MVR, and thus symptoms cannot be attributed to the severity of MVR alone. Further, women with FMV/MVP syndrome, symptoms at least partially may be related to β1-adrenergic receptor polymorphism, which has been shown previously to be associated with a hyperresponse to adrenergic stimulation

775-2 Deleterious Effect of Smoking on the Elastic Properties of the Aorta

Cigarette smoking alters vascular reactivity and thus may alter the elastic properties of the aorta (Ao). To test this hypothesis, serial pressure-diameter loops (figure A) were obtained from the simultaneous recordings of the thoracic Ao diameter (D) and pressure (P) before and atterthe initiation of smoking of one cigarette (nicotine content 1.3mg) in 20 healthy smokers who underwent diagnostic cardiac catheterization. Ao 0 were measured by a Yshaped catheter, developed in our institution, which incorporates at its distal tips a pair of ultrasonic dimension crystals (Crystal Biotech, MA). This highdefinition diameter gauge was validated in in-vitro and experimental studies. Ao Pwere recorded by a Millar micromanometer. The pressure-diameter relationship changed significantly with smoking (figure A). Ao distensibility (=2Δd/dx ΔP, where Δd and ΔP: changes from systole to diastole of the Ao D and P respectively, and d: diastolic Ao D) was decreased significantly after smoking (figure B). These changes suggest that the Ao became stiffer atter smoking.This effect of smoking on the elastic properties of the aorta adds to the multiple other deleterious effects of smoking on human health

The endlessness evolution of medicine, continuous increase in life expectancy and constant role of the physician

In this review, the endlessness evolution of medical science and medical technology, and its effects on disease metamorphosis and increased life expectancy are discussed. In certain instances, the past will be compared with the present and predictions for the future will be outlined. Further, the constant role of the physician in maintaining the health of human beings is emphasized in this endlessness evolution. (C) 2017 Hellenic Society of Cardiology. Publishing services by Elsevier B.V

Floppy Mitral Valve (FMV) – Mitral Valve Prolapse (MVP) – Mitral Valvular Regurgitation and FMV/MVP Syndrome

Mitral valve prolapse (MVP) results from the systolic movement of a portion(s) or segment(s) of the mitral valve leaflet(s) into the left atrium during left ventricular (LV) systole. It should be emphasised that MVP alone, as defined by imaging techniques, may comprise a non-specific finding because it also depends on the LV volume, myocardial contractility and other LV hemodynamics. Thus, a floppy mitral valve (FMV) should be the basis for the diagnosis of MVP. Two types of symptoms may be defined in these patients. In one group, symptoms are directly related to progressive mitral regurgitation and its complications. In the other group, symptoms cannot be explained only by the degree of mitral regurgitation alone; neuroendocrine dysfunction has been implicated for the explanation of symptoms in this group of patients that today is referred as the FMV/MVP syndrome. When significant mitral regurgitation is present in a patient with FMV/MVP, surgical intervention is recommended. In patients with a prohibitive risk for surgery, transcatheter mitral valve repair using a mitraclip device may be considered. Furthermore, transcatheter mitral valve replacement may represent an option in the near future as clinical trials are underway. In this brief review, the current concepts related to FMV/MVP and FMV/MVP syndrome will be discussed

The Cardio-Renal Interrelationship

The heart and the kidney are of utmost importance for the maintenance of cardiovascular (CV) homeostasis. In healthy subjects, hemodynamic changes in either organ may affect hemodynamics of the other organ. This interaction is fine-tuned by neurohumoral activity, including atrial natriuretic peptides, renin-angiotensin aldosterone system and sympathetic activity. Dysfunction or disease of one organ may initiate, accentuate, or precipitate dysfunction or disease state in the other organ, often leading to a vicious cycle. Further, the interaction between the heart and the kidney may occur in the setting of processes and diseases that may affect both organs simultaneously, such as advanced age, hypertension, diabetes mellitus, atherosclerosis, etc. In this regard, a stiff aorta that occurs with aging due to mechanical stress may independently initiate or precipitate dysfunction and disease in the heart and the kidney. All of these factors contribute to a high prevalence of coexistent CV and kidney disease, especially in the elderly. In advanced kidney disease, hemodynamic and neurohumoral homeostasis are lost, volume and pressure overload may coexist, and the elimination of certain pharmacologic agents may be substantially impaired. Thus, coexistence of CV and kidney disease complicates diagnosis, propagates pathophysiology, adversely affects prognosis, and hinders management. (C) 2016 Elsevier Inc. All rights reserved