Mitral valve prolapse. A common cardiac diagnosis in women.

Mitral Valve Prolapse (MVP) is the most frequently diagnosed cardiac valvular abnormality. It is a primary disorder with familial occurrence. MVP is a disease of the young with a significantly higher incidence in women compared to men. The most characteristic clinical finding is a midsystolic click and late systolic murmur detected on cardiac auscultation. Two-dimensional echocardiography is the diagnostic tool of choice. 2D echo also helps in stratification of MVP patients at risk of developing serious complications. Although MVP runs a benign course in the majority of patients, significant complications may occur. These include progressive mitral regurgitation with heart failure, infective endocarditis, systemic emboli, cardiac arrhythmias, and rarely sudden death. The focus of therapy is reassurance and symptom relief when possible. It is important to recognize those patients that are at risk of developing significant complications, follow them closely, and intervene appropriately when complications occur.

Comparative effects of propranolol and diltiazem on systolic and diastolic left ventricular function in essential hypertension.

The effects of propranolol and diltiazem on left ventricular systolic and diastolic function in hypertensive subjects (DBP 90-114 mmHg) were examined with M-mode and 2D echocardiograms in 21 patients in a double-blind fashion prior to and after 4 months of treatment. Systolic function was assessed by measurement of fractional shortening, mean velocity of fibre shortening, peak systolic pressure/end systolic dimension ratio, and end systolic stress/end systolic dimension ratio. To assess diastolic function, maximal rate of change in left ventricular dimension (MAXD), maximal rate of change in posterior wall thinning (MAX PWT) and early diastolic (EDD) and late diastolic dimension changes (LDD) were calculated using digitised M-mode images of mid-wall diameter. Both propranolol and diltiazem reduced systolic and diastolic pressures similarly. No significant changes were observed in any of the parameters of systolic function with either drug. Similarly neither propranolol nor diltiazem altered MAXD or EDD significantly. Although changes in maximal rate of posterior wall thinning (MAX PWT) were not significant with either drug, diltiazem improved MAX PWT in 7 of 8 patients. The results of the study demonstrate that both propranolol and diltiazem reduce blood pressure without significant deleterious effects on systolic or diastolic function. Diastolic functional parameters, which were not abnormal at baseline, showed no consistent change with either propranolol or diltiazem.

The central hemodynamics of severe preeclampsia.

Swan-Ganz hemodynamic monitoring in 49 antepartum patients with severe preeclampsia revealed a variable hemodynamic profile. The majority of patients had normal left ventricular filling pressure (8.4 +/- 0.2 mm Hg), normal to high cardiac index (4.4 +/- 0.1 L.min-1.m2), and upper normal to moderately elevated systemic vascular resistance (1226 +/- 37 dynes.sec.cm-5). Eight patients had pulmonary edema and their findings included high wedge pressure (18 +/- 1 mm Hg), upper normal to high cardiac index (4.9 +/- 0.5 L.min-1.m2), and normal systemic vascular resistance (964 +/- 50 dynes.sec.cm-5). Left ventricular function was hyperdynamic in 73% of the 49 patients. Patients with chronic hypertension and superimposed preeclampsia were hemodynamically indistinguishable from patients with preeclampsia alone. We conclude that, in general, preeclampsia is a high cardiac output state associated with an inappropriately high peripheral resistance. The normal wedge and central venous pressures suggest central redistribution of intravascular volume if the generally accepted reports of decreased plasma volume in preeclampsia are correct.

Circulatory congestion in obese hypertensive women: a subset of pulmonary edema in pregnancy.

We describe four obese, chronically hypertensive women presenting with antepartum pulmonary edema in whom invasive hemodynamic monitoring showed elevated wedge pressure, normal to high cardiac index, and normal systemic vascular resistance. Echocardiography revealed large chambers, thick walls, and increased left ventricular mass with normal systolic but abnormal diastolic function. These findings are indicative of intrinsic volume overload occurring in the presence of impaired left ventricular relaxation, a combination resulting in high filling pressures and pulmonary congestion. Diuretic therapy is indicated in this subset of patients, who could not be recognized by the usual clinical parameters such as history and physical examination, chest x-ray, and arterial blood gas.

Sodium sensitivity in human subjects. Hemodynamic and hormonal correlates.

To investigate factors associated with sodium sensitivity, 157 subjects were studied while receiving 10 and 200 mEq sodium diets. Measurements included blood pressure (BP), forearm vascular resistance, plasma renin activity (PRA), and plasma aldosterone. Sodium repletion was associated with a greater than 5% increase in mean BP in 16% of the normotensive subjects and 29% of the borderline hypertensive subjects. Sodium-sensitive subjects were compared with sodium-resistant subjects in both the normotensive (n = 92) and borderline hypertensive (n = 65) groups. Forearm vascular resistance was significantly higher (p less than 0.05) during sodium loading in the sodium-sensitive subgroups of both the normotensive and borderline hypertensive groups (35.8 +/- 29 vs 23.8 +/- 20 [SD] and 37.5 +/- 29 vs 22.5 +/- 14 mm Hg/ml/min/100 g, respectively. Venous capacitance was lower in the sodium-sensitive than in the sodium-resistant borderline hypertensive subjects (0.8 +/- 0.21 vs 1.69 +/- 0.24 ml/100 g). During sodium restriction, PRA was significantly lower (p less than 0.01) in the sodium-sensitive subsets (2.56 +/- 1.6 vs 4.04 +/- 2.6; 2.65 +/- 2.1 vs 3.88 +/- 2.6 ng angiotensin I/ml/hr). Aldosterone was lower (p less than 0.01) during sodium depletion in the sodium-sensitive subsets (17.3 +/- 12 vs 26.3 +/- 16; 18.5 +/- 18 vs 27.9 +/- 17 ng/ml). A significant inverse correlation existed between change in BP with sodium repletion and change in PRA or level of PRA during sodium depletion (p less than 0.003).(ABSTRACT TRUNCATED AT 250 WORDS)

Sodium sensitivity in normotensive and borderline hypertensive humans.

The responses to sodium depletion and repletion were studied in subgroups of 92 normotensive and 65 borderline hypertensive individuals. The borderline hypertensives were characterized by significantly higher blood pressure, weight, cardiac output, hematocrit and decreased density of conjunctival capillaries and venules. Sodium-sensitivity was defined as an increase in mean arterial blood pressure exceeding 5% during sodium repletion. The prevalence of sodium-sensitivity was higher in blacks than in whites and greater in hypertensives than in normotensives. Sodium-sensitive individuals were characterized by significantly increased forearm vascular resistance and decreased plasma renin activity and aldosterone concentration. The resemblance of these changes to those reported in the Dahl salt-sensitive rat suggests a genetic basis for the response to sodium.

Acquired left ventricular to coronary sinus fistula: an unusual complication of acute myocardial infarction.

Anatomical complications of myocardial infarction include ventricular septal defect and mitral regurgitation. Another unusual complication of myocardial infarction is described, and its diagnosis and surgical management are discussed.

Hemodynamic characteristics of sodium-sensitive human subjects.

Fifty-eight normal subjects and 51 subjects with borderline hypertension underwent microvascular and hemodynamic studies while on an ad libitum diet and during periods of sodium depletion (10 mEq/day) and repletion (200 mEq/day). Hemodynamic measurements included arterial blood pressure, cardiac index, total peripheral resistance, forearm blood flow, vascular resistance, venous compliance, and capillary filtration fraction. Studies of the microcirculation consisted of macrophotography of the bulbar conjunctiva with measurement of anteriolar, venular, and capillary density and diameter. During sodium repletion, cardiac index increased significantly in the normal subjects (2.35 +/- 0.7 vs 2.44 +/- 0.7 L/min/m2; p less than 0.01) and in the borderline hypertensive subjects (2.50 +/- 0.7 vs 2.70 +/- 0.8 L/min/m2; p less than 0.01). However, mean blood pressure rose by more than 5% in only 33 subjects, 13 with normal and 20 with borderline hypertension. When these sodium-sensitive subjects were compared with those whose blood pressure did not rise, the former were found to have significantly higher forearm vascular resistance (32.2 +/- 21 vs 17.9 +/- 12 mm Hg/ml/min/100 g; p less than 0.01), lower forearm blood flow (4.42 +/- 2.7 vs 7.47 +/- 5.0 ml/min/100 g) and lower conjunctival capillary density (3.72 +/- 1.7 vs 5.18 +/- 2.1 [SD] mm/mm2; p less than 0.05). These results indicate that sodium sensitivity in humans is accompanied by elevation of forearm vascular resistance and attenuation of the microcirculation.

Underlying cardiac lesions in adults with infective endocarditis. The changing spectrum.

The spectrum of recognized cardiac lesions underlying infective endocarditis has been changing as a result of the decline in incidence of rheumatic heart disease, the recognition of the entity of mitral valve prolapse, and the improvement in cardiac diagnostic techniques. Sixty-three cases of native valve endocarditis diagnosed in Memphis hospitals between 1980 and 1984 were reviewed. All diagnoses of underlying cardiac lesions were confirmed by two-dimensional echocardiography, cardiac catheterization, and/or histopathologic examination of valve tissues. Major categories of underlying lesions were as follows: mitral valve prolapse, 29 percent; no underlying disease, 27 percent; degenerative lesions of the aortic or mitral valve, 21 percent; congenital heart disease, 13 percent; rheumatic heart disease, 6 percent. Thus, mitral valve prolapse and, in the elderly, degenerative lesions have displaced rheumatic and congenital heart diseases as the major conditions underlying endocarditis. Redundancy of the mitral valve leaflets was noted in 17 of 18 patients in whom endocarditis was superimposed upon mitral valve prolapse. The risk of infective endocarditis appears to be substantially increased in the subset of patients with mitral valve prolapse who exhibit valvular redundancy.

Mitral valve prolapse in women with oral contraceptive-related cerebrovascular insufficiency. Associated persistent hypercoagulable state.

We examined a group of former oral contraceptive (OC) users, who had experienced cerebrovascular insufficiency, for the presence of hypercoagulable states. We found hypercoagulability in this group in the form of decreased plasma antithrombin III activity, increased platelet coagulant activity, and elevated plasma beta-thromboglobulin level. Certain characteristics (cigarette smoking, vascular headache, hyperlipidemia, and mitral valve prolapse) were encountered with increased frequency among former OC users who had experienced cerebrovascular insufficiency. The association of mitral valve prolapse with OC-related cerebrovascular insufficiency was particularly striking. We propose that preexisting hypercoagulable states, such as may exist in a subset of individuals with mitral valve prolapse, will magnify the risk of OC-related cerebrovascular morbidity.

Evidence for altered vascular reactivity in sodium-sensitive young subjects with borderline hypertension.

To assess mechanisms associated with the pressor effects of a high sodium diet in susceptible individuals, the hemodynamic and hormonal effects of sodium depletion and repletion were studied in 33 normal subjects and 30 subjects with borderline hypertension. The hypertensive group had significantly higher mean arterial pressure, weight, hematocrit, and upright plasma renin activity. Forearm hemodynamics were measured during periods of ad lib diet, 10 mEq, and 200 mEq sodium diet. The fall in forearm resistance during reactive hyperemia was inversely related to mean arterial pressure at rest (R = .400, p less than .005) and rose significantly in hypertensive subjects during salt depletion, 39 +/- 3.6 to 61 +/- 6.1 mmHg/ml/min/100 g (p less than .05). Sodium sensitivity in either normotensive or borderline hypertensive subjects was defined as an increase in mean blood pressure of more than 5% when sodium repleted. The individuals who were sodium sensitive had a higher forearm vascular resistance during sodium depletion than those who were sodium resistant, 67 +/- 10.5 versus 45 +/- 4.1 mm/ml/min/100 g (p less than .03). We conclude that young individuals with borderline hypertension already have alterations in vascular reactivity. This trait is shared by normotensive individuals whose blood pressure rises in response to sodium.

Hemodynamic mechanisms of adaptation to chronic high sodium intake in normal humans.

The long-term hemodynamic effects of a high dietary sodium intake were studied in 10 young normal subjects. After a 4-day diet of 10mEq of sodium and 60 mEq of potassium per day the mean arterial blood pressure (MAP) was 82.3 +/- 15.1 mmHg, the cardiac index (CI) was 2.32 +/- 0.69 liter/min/m2, and total peripheral resistance (TPR) was 1778 +/- 947 dyne sec cm-5. After 4 to 6 days of 200 mEq of sodium and 60 mEq of potassium per day, MAP was 84.3 +/- 20.9 mm Hg, CI had risen to 2.53 +/- 0.61 liter/min/m2, and TPR fell to 1437 +/- 328 dyne sec cm-5. After 6 months of unrestricted sodium intake, urinary sodium excretion (UNa) was 144.1 +/- 51.9 mEq/24 hrs (p less than 0.001), MAP remained at 83.1 +/- 13.8 mm Hg, CI had risen to 3.11 +/- 1.01 liter/min/m2 (p less than 0.05) and TPR was 1268 +/- 444 dyne sec cm-5. After 12 months, UNa had risen to 171.5 +/- 97.6 mEq/24 hrs (p less than 0.005), while MAP remained at 82.4 +/- 17.9 mm Hg, CI at 3.08 +/- 1.16 liter/min/m2 (p less than 0.05), and TPR at 1282 +/- 500 dyne/sec/cm-5. Thus, cardiac index rises significantly with sodium intake in normal subjects and remains at a higher level for as long as 12 months. Blood pressure does not rise because TRP falls proportionately.

Long-term captopril therapy: evolving hemodynamic effects.

Nine patients with resistant hypertension received captopril for 12 months. Five received captopril alone, four required additional therapy. In the former, mean blood pressure fell from 109 +/- 4.2 mm Hg to 84 +/- 7.5 mm Hg (P less than 0.025) after seven days. A rise to 101 +/- 19 mm Hg was noted at six and 12 months. Total peripheral resistance fell at seven days but returned to levels above control at six and 12 months. Cardiac index was 3.21 +/- 0.55 liters/min/m2 before treatment, 3.27 +/- 0.56 liters/min/m2 at seven days, and 2.17 +/- 4.0 liters/min/m2 (P less than 0.025) at 12 months. However, forearm blood flow rose from subnormal levels during the 12 months of observation, suggesting a persistent effect on the arterioles of the extremities. Plasma converting enzyme activity was significantly reduced at seven days but was above control levels at six and 12 months. However, plasma renin activity remained elevated, and plasma aldosterone concentration was significantly reduced. The fall in mean blood pressure was not related to the change in plasma converting enzyme activity in patients receiving captopril alone (five patients) or with diuretic (two patients). In the presence of beta-adrenergic blockade and volume depletion (two patients), changes in mean blood pressure appeared to be related to changes in converting enzyme activity. The data suggest that patients with essential hypertension whose blood pressure was not adequately controlled by previous medications may initially respond to captopril with a fall in blood pressure and total peripheral resistance. However, in certain individuals, these effects diminish with time despite addition of diuretics and beta-adrenergic receptor blocking agents.

The effect of diet on echocardiographic left ventricular dimensions in normal man.

The effect of dietary sodium and potassium on echocardiographic left ventricular dimensions was studied in normal subjects. In 10 subjects, left ventricular end diastolic volume was found to be 18.8 greater, and systolic volume 17.1% higher with zoo mEq sodium diet than on a 1Omeq sodium diet (P less than 0.025). While receiving an ad libitum diet, the subjects were found to have an end diastolic volume of 107.9 +/- 6.4 ml SE and an end systolic volume of 45.2 +/- 2.7 ml SE. During sodium depletion, values fell to 101.3 +/- 5.7 ml SE and 38.6 +/- 2.9 ml SE, respectively, then on a high sodium diet rose to 120.3 +/- 7.0 ml SE and 45.2 +/- 2.7 ml SE, respectively. Heart rate fell during sodium repletion by 4.2% (P less than 0.05) while mean arterial blood pressure, cardiac output and peripheral vascular resistance did not change significantly. In contrast, seven subjects consuming a diet containing 25 and 200 mEq potassium in seqeucne, the sodium intake remaining constant, did not display significant changes in cardiac dimension, heart rate, blood pressure, cardiac output, or vascular resistance. It is concluded that dietary sodium significantly effects the size of a nonfailing left ventricle, an effect that must be considered when single or sequential echocardiograms are interpreted.

Short-term therapy of severe hypertension. Hemodynamic correlates of the antihypertensive response in man.

Ten severely hypertensive patients were randomized into five treatment groups: vasodilators; vasodilators plus diuretics; sympatholytics; sympatholytics plus diuretics; and sympatholytics, diuretics, and vasodialtors. Cardiac index was measured daily by echocardiography, and total peripheral resistance (TPR) calculated. Plasma renin activity (PRA) and creatinine clearance (CCR) were measured every other day. There was no difference in antihypertensive response. Seven patients, whose initial TPR was high, responded to treatment with a fall in TPR, regardless of regimen. Three patients with a high pretreatment cardiac index responded with a fall in cardiac index. Changes in TPR or cardiac index were not related to changes in CCR. There was no correlation between PRA and either blood pressure or TPR. It is concluded that the pretreatment hemodynamic status of severely hypertensive patients is the major determinant of the hemodynamic response to antihypertensive therapy.

Hemodynamic and antihypertensive effects of captopril, an orally active angiotensin converting enzyme inhibitor.

Captopril inhibits angiotensin II formation and bradykinin degradation in vivo. Eleven patients with essential hypertension (EH) and four patients with renovascular hypertension (RVH) were treated with captopril for periods ranging from 3 days to 12 months. All patients had a diastolic blood pressure (DBP) over 95 mm Hg after receiving a placebo for 3 days. Captopril given in ascending doses (10-1000 mg/day) caused normalization of blood pressure in all but three patients, one with severe RVH whose pressure fell 11%, one patient with severe EH, whose pressure fell 27%, and one with EH whose blood pressure fell 8.5%. The average control DBP in patients with EH was 113.7 +/- 5.5 (SE) mm Hg and fell to 89.9 +/- 3.6 mm Hg (p less than 0.001), while DBP in patients with RVH fell from 110.7 +/- 7.6 mm Hg to 94.5 +/- 8.2 (p less than 0.005). All patients were studied in balance on a 100 mEq sodium (Na) diet. Plasma renin activity (PRA) versus 24-hour urinary Na excretion increased sevenfold during therapy while converting enzyme activity fell by about one half. The magnitude of the blood pressure response was not related to control PRA. Cardiac output was estimated by echocardiography during placebo administration and during maintenance therapy with captopril. A significant change was not observed. Total peripheral resistance fell an average of 18.9% (p less than 0.05) in 11 of the 13 patients in whom the measurement could be made. It is concluded that captopril effectively lowers blood pressure in patients with EH or RHV by reducing total peripheral resistance.

SQ 20,881: effect on eclamptic--pre-eclamptic women with postpartum hypertension.

The renin-angiotensin system has been implicated in the genesis of pre-eclampsia. To avoid fetal toxicity, five women were studied who developed hypertension, proteinuria, and edema in the last trimester of pregnancy and whose BP elevation persisted immediately postpartum. At about 6 hours after delivery the CE enzyme inhibitor (SQ 20,881) was given in incremental doses ranging from 0.25 to 3.0 mg. per kilogram intravenously, before and after diuresis with furosemide, 40 mg. intravenously. BP was measure every 2 minutes and PRA and angiotensin II concentration before treatment, 30 minutes after 0.25 to 0.30 mg. per kilogram, and 30 minutes after 2.0 to 3.0 mg. per kilogram. Echocardiographic assessment of CI and PVR was performed before treatment and after a maximum dose in three patients. Before diuresis, CE blockade had no effect on heart rate, BP, CI, PVR, or PRA, regardless of whether the patient was in positive or negative fluid balance or was sodium loaded or restricted over the preceding 24 hours. Angiotensin II fell by 77 and 10 per cent, respectively, after 0.25 mg. per kilogram was given to two patients, but rose slightly in the other three patients, then fell an average of 46 per cent after 1.0 to 3.0 mg. per kilogram were given. After diuresis, 1.0 mg. per kilogram resulted in a 24 per cent fall in BP which persisted for 3 hours in two patients and a 14 per cent fall which lasted for 30 minutes after 1.0 or 3.0 mg. per kilogram in a third patient. It is concluded that the BP elevation which persists after delivery in certain patients with pre-eclampsia is not angiotensin II dependent.