Heart rate and blood pressure in mitral valve prolapse patients: divergent effects of long-term propranolol therapy and correlations with catecholamines.

OBJECTIVE: There is a well known association between mitral valve prolapse (MVP) and low blood pressure (BP), although patients often have high levels of catecholamines and high heart rate (HR). The main objective of our study was to evaluate the effects of long-term adrenergic beta-blockade on these parameters. METHODS: The study population consisted of 46 patients with MVP and the control group consisted of 20 normal individuals. The study had two phases: in the first phase, patients were free of medications. In the second phase, patients were under treatment with propranolol for 10 to 12 months. The tests were performed in normal individuals and patients in the first phase. Only patients underwent the same tests in the second phase. Measurement of urinary epinephrine and norepinephrine levels, by high performance liquid chromatography, was done. Rest HR was determined by electrocardiogram (ECG), and ambulatory blood pressure and HR were evaluated by 24 hours ambulatory blood pressure monitoring (ABPM) using the auscultatory method. RESULTS: The levels of epinephrine and norepinephrine were significantly higher in patients than in normal controls and decreased under propranolol. Rest and ambulatory HR were higher in patients and decreased under propranolol. The 24 hours systolic and diastolic BPs were lower in patients, and their values increased under propranolol. Heart rate decreasing and epinephrine levels reduction were positively correlated. No correlation was found between BP increase and catecholamine levels. CONCLUSION: The study results show divergent effects of propranolol on blood pressure, which increased, and on heart rate, that decreased, in patients with MVP. Heart rate decrease was an expected result and depends, namely, on b1 receptors blockade. Increase in BP is an unusual response to adrenergic beta-blockade in normal conditions, and this finding supports the preponderance of b2 receptors on the BP control in patients with MVP.

Symptomatic mitral valve prolapse in children and adolescents: catecholamines, anxiety, and biofeedback.

It has been proposed that symptomatic mitral valve prolapse may be associated with a hyperadrenergic state and/or increased anxiety. To test this hypothesis, Spielberger State-Trait Anxiety (STAI) scores and 24-hour urinary catecholamine collections were gathered from 11 children and adolescents without mitral valve prolapse, 6 with asymptomatic mitral valve prolapse, and 14 who had chest pain (some with additional symptoms of shortness of breath, palpitations, and fatigue). STAI scores and catecholamine excretion values were not significantly different between groups. Ten symptomatic patients were randomly assigned to either eight sessions of skin temperature biofeedback with daily home practice of relaxation-mental imagery techniques or an attention-placebo condition. Change in 24-hour urinary catecholamine excretion values and STAI scores from baseline to end of treatment did not differ significantly between treatment and placebo conditions. Although not evident at the end of treatment, a significant decrease in chest pain was found in the biofeedback group at 6-month follow-up evaluation. In summary, results of this study did not show evidence of increased sympathetic tone or levels of anxiety in symptomatic pediatric patients with mitral valve prolapse. A behavioral treatment program using biofeedback and relaxation-mental imagery techniques was associated with decreased chest pain at 6-month follow-up.

Renal excretion of lactate and magnesium in mitral valve prolapse.

A strong positive correlation between urinary magnesium and lactate was found in 17 magnesium-depleted patients with echocardiographically proved mitral valve prolapse. The strong correlation over all the range of urinary magnesium values and the significantly increased excretion of lactate suggest urinary magnesium loss in this syndrome.

Associations among serum N-terminal procollagen type III concentration, urinary aldosterone-to-creatinine ratio, and ventricular remodeling in dogs with myxomatous mitral valve disease.

OBJECTIVE: To assess relationships among serum N-terminal procollagen type III concentration, urinary aldosterone-to-creatinine concentration ratio (UAC), and clinical variables in dogs with myxomatous mitral valve disease (MMVD) and healthy dogs. ANIMALS: 162 dogs with MMVD and 24 healthy control dogs of comparable age and body weight. PROCEDURES: Blood and urine samples were collected from each dog. Dogs with MMVD underwent echocardiography and ECG. Ventricular diameter measurements were normalized for body weight. Serum N-terminal procollagen type III and urinary aldosterone concentrations were measured via radioimmunoassay. Each dog was examined on 1 to 3 occasions. Examinations were repeated at approximately 6-month intervals. RESULTS: Serum N-terminal procollagen type III concentration decreased with increasing severity of MMVD and was negatively associated with age and left ventricular end-diastolic and end-systolic diameters. The UAC increased with prior percentage change in left ventricular end-diastolic diameter per month, subsequent percentage change in left ventricular end-systolic diameter per month, and treatment with diuretics and was negatively associated with age. Both UAC and serum N-terminal procollagen type III concentration were higher in Cavalier King Charles Spaniels than in other breeds when other measured variables were controlled for. CONCLUSIONS AND CLINICAL RELEVANCE: In dogs with MMVD, echocardiographic indicators of left ventricular remodeling appeared to be associated with a decrease in serum concentration of a marker of collagen type III turnover and an increase in urinary aldosterone concentration.

The mitral valve prolapse syndrome.

In clinical perception, the syndrome has evolved from a neuropsychiatric disorder to a medical disease with an anatomic basis. Still unanswered is whether the autonomic and adrenergic dysfunctions that occur in some patients are an intrinsic part of the syndrome or of an unrelated anxiety neurosis. Pending clarification, both medical and psychological aspects require attention.