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10 Groupe de recherche PACTE. Prevention des accidents thrombo-emboliques systemiques chez les porteurs de protheses valvulaires artificielles: essai cooptratif control& du dipyridamole. Coeur 1978;9:915-969. 11 Dale J. Myhre E, Storstein 0, Stormorken H, Efskind L. Prevention of arterial thromboembolism with acetylsalicylic acid. A controlled clinical study in patients with aortic ball valves. Am Heart J 1977;94:101-111. 12 Altman R, Boullon F, Rouvier J, Rata R, De la Fuente L, Favaloro R. Aspirin and prophylaxis of thromboembolic complications in patients with substitute heart valves. J Thorac Cardiovasc Surg 1976;72:127-129. 13 Dale J, Myhre E. Can acetylsalicylic acid alone prevent arterial thromboembolism? A pilot study in patients with aortic ball valve prostheses. Acta Med Stand 1981;645:73-78. 14 Brott WH, Zajtchuk R, Bowen TE, Davis J, Green DC. Dipyridamole - aspirin as thromboembolic prophylaxis in patients with aortic valve prosthesis. J Thorac Cardiovasc Surg 1981;81:632-635. 15 Wessler S, Gitel S. Rethrombosis - warfarin or low-dose heparin? N Engl J Med 1979;301:889-891. 16 Blanchard RA, Furie BC, Kruger SF, Furie B. Plasma prothrombin and abnormal prothrombin antigen: correlation with bleeding and thrombotic complications in patients treated with warfarin. Blood 1981;58:231a.
Is left ventricular dysfunction present in patients with atrial septal defect and signs and symptoms of left-sided heart failure? Atria1 septal defect, although tolerated by patients for several years is sometimes associated with symptoms of left ventricular failure. Dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea may be seen late in the disease. These symptoms coupled with the findings of depressed left ventricular cardiac output at increased left ventricular filling pressures suggested that left ventricular dysfunction was present in some patients with atria1 septal defect [l-4]. While atria1 septal defect produces volume overload of the right ventricle it produces no obvious overload on the left ventricle. Thus a cause for the proposed left ventricular dysfunction has remained obscure. Recent studies of left ventricular function in patients with atria1 septal defect have found normal or only mild abnormalities in systolic function [S-7]. However, none of these studies examined left ventricular function in atria1 septal defect patients who specifically had symptoms of left ventricular failure where left ventricular dysfunction might likely be present. An attempt to resolve the issue We examined hemodynamic data and left ventricular mechanics in patients with atria1 septal defect who had symptoms and physical signs of /ef? ventricular failure and compared these findings to patients with atria1 septal defect without failure symptoms and to normal patients [8]. The heart failure-atria1 septal defect group consisted of 6 patients who had at least three of the four following criteria: dyspnea on exertion, orthopnea, paroInternational Journal of Cardiology, 0 Elsevier Science Publishers
3 (1983) 91-94
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EJECTION FRACTION
Vcf
60
1.6
30
1.4
.60
ESWESVI
1.2
50
: P ” .k o
.40 30
1.0 6 .6
.20
.4
.I0
.02 NORMALS
ASO-CMF
NASD
NORMALS
ASO-CHF
NASD
NORMALS
ASD-CHF
NASD
Fig. Ejection fraction, mean velocity of circumferential fiber shortening (Vcf) and the end-systolic stress-end-systolic volume index (ESS/ESVI) are shown for normal individuals, patients with atria1 septal defect and heart failure (ASD-CHF) and atria1 septal defect patients without heart failure (NASD). There were no differences in these measures of left ventricular function in these three groups.
xysmal nocturnal dyspnea and a third heart sound heard over the left ventricular apex. The non-failure group consisted of 12 patients who were asymptomatic (7 patients) or who had only mild dyspnea on exertion (2 patients) or only palpitations (3 patients). Right- and left-sided heart catheterization was performed in these 18 patients with atria1 septal defect. All underwent left ventriculography. Intracardiac pressures measured in the failure-atria1 septal defect group were consistently elevated compared to the non-failure group and to known normal values. The average left ventricular end-diastolic pressure in the failure group was 17 -I_0.8 mmHg compared to the non-failure group (6.9 + 0.6 mmHg) P < 0.001. Mean right atria1 pressure was 11.0 & 1.3 mmHg in the heart failure group versus 4.9 + 0.5 mmHg in the non-failure group P -c 0.001. Pulmonary artery pressure was likewise elevated in the failure group (30 + 1.8 mmHg) versus 15 + 1.0 mmHg in the non-failure group P -c 0.001. Cardiac index and the amount of left to right shunting were not significantly different in the two groups of patients with atria1 septal defect. In contradistinction, various indices of left ventricular systolic function were similar both in the failure and non-failure atria1 septal defect groups and in normal individuals. As shown in the Figure, ejection fraction, mean velocity of circumferential fiber shortening and the ratio of end-systolic stress to end-systolic volume index were similar in all three groups examined. Systolic function is normal Although clear abnormalities in left ventricular hemodynamics exist in some patients with atria1 septal defect, global contractile function was normal in both groups of patients with atria1 septal defect. Ejection fraction was normal even in the group of patients with symptoms of heart failure and elevated filling pressures. Mean velocity of circumferential fiber shortening and the ratio of end-systolic stress to end-systolic volume [9] are more independent of load conditions than ejection fraction and thus more reflective of
93
true contractile function. These indices also were normal in the heart failure-atria1 septal defect group and similar to the non-failure group. Thus, while the increased filling pressure noted in our failure group probably accounts for the symptoms encountered and the presence of the third heart sounds heard, the elevation of filling pressures is not secondary to any significant global systolic malfunction. A diastolic abnormality is probable Although our study did not specifically examine left ventricular diastolic properties, a diastolic abnormality can be postulated to explain our findings since global systolic function was normal. The volume overload to the right ventricle seen in atria1 septal defect could alter the filling properties of the left ventricle and reduce left ventricular compliance [lo]. In right ventricular volume overload the interventricular septum may be shifted leftward, reducing left ventricular chamber size thus making left ventricular filling more difficult. Secondly, both ventricles are, of course, enclosed by a common pericardium. Increased right ventricular volume may encroach upon filling of the left ventricle via the pericardium. As the enlarged right ventricle takes up volume inside the non-compliant pericardium it restricts left ventricular volume and reduces chamber compliance. In summary, patients with atria1 septal defect may develop symptoms and signs of left ventricular failure. Elevated left ventricular filling pressures in part account for these signs and symptoms. While left ventricular filling pressures may be elevated and cardiac output reduced in patients with atria1 septal defect, these findings are best explained by reduced left ventricular chamber compliance since global systolic function is normal. Temple University Hospital 3401 N. Broad Street Philadelphia, PA 19140, U.S.A.
Blase A. Carabello James F. Spann References
1 Flamm MD, Cohn KE, Hancock EW. Ventricular function in atria1 septal defect. Am J Med 1970;48:286-94. 2 Dexter L. Atrial septal defect. Br Heart J 1956;18:209-25. 3 Tikoff G, Keith TB, Nelson RM, Kuda H. Clinical and hemodynamic observations after surgical closure of large atrial septal defect complicated by heart failure. Am J Cardiol 1969;23:810-7. 4 Epstein SE, Beiser DG, Goldstein RE, Rosing DR, Redwood DR, Morrow AG. Hemodynamic abnormalities in response to mild and intense upright exercise following operative correction of an atrial septal defect or tetralogy of Fallot. Circulation 1973;47: 1065-75. 5 St John Sutton MG, Tajik AJ, Mercier L, Seward JB, Giuliani ER, Ritman EL. Assessment of left ventricular function in secundum atria1 septal defect by computer analysis of the M-mode echocardiogram. Circulation 1979;60: 1082-90. 6 Popio KA, Gorlin R, Teichholz LE, Cohn PF, Bechtel D, Herman MV. Abnormalities of left ventricular function and geometry in adults with an atria1 septal defect. Am J Cardiol 1975;36:302-8. 7 Bonow RO, Borer JS, Rosing DR. Bacharach SL, Green MV, Kent KM. Left ventricular function reserve in adult patients with atrial septal defect: pre and post operative studies. Circulation 1981:63:1315-22.
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8
Carabello BA, Gash A, Mayers D, Spann JF. Normal left ventricular
systolic function in adults with atria1 septal defect and left heart failure. Am J Cardiol 1982;49: 1868-73. 9 Carabello BA. Nolan SP, McGuire LB. Assessment of preoperative left ventricular function in patients with mitral regurgitation: value of the end systolic wall stress - end systolic volume ratio. Circulation 1981;64:1212-17. 10 Bemis CE. Serur JR, Borkenhagen D, Urschel CW. Influence of right ventricular filling pressure on left ventricular pressure and dimension. Circ Res 1974;34:498-504.
Cardiovascular adaptations to obesity and arterial hypertension: detrimental or beneficial? The hypertension-obesity
connection
Obesity is one of the most prevalent disorders in westernized societies. More than one-third of Americans between 40 and 49 years of age are at least 20% overweight. Numerous studies have documented that high blood pressure and obesity frequently coexist in the same patient [l]. Unfortunately, physicians often consider one as the innocent bystander of the other, perhaps because no single reason for their common association has been found. Three epidemiologic observations link hypertension with obesity: (1) normotensive obese patients have a high risk of developing hypertension; (2) lean hypertensive patients have a tendency to become overweight; (3) weight loss commonly reduces arterial pressure even when the patient does not restrict his or her salt intake. Despite the innocent bystander concept that most physicians have, the association of hypertension with obesity is by no means a simple one. While the two evils may potentiate some cardiovascular abnormalities, their combined presence may also offset others [2]. Cardiac changes with obesity Obesity is defined by an excessive amount of fat tissue that increases total body oxygen consumption and thus, in turn, requires an increment in cardiac output [3,4]. Since heart rate remains unchanged, the elevated cardiac output results from an TABLE
1
Left ventricular
Cardiac output Contractility Preload Afterload Stroke work
function. Obesity
Hypertension
t I tr t t
_ t _ tt t
International Journal of Cardiology, 3 ( 1983) 94-97 0 Elsevier Science Publishers