Afterload reduction in the management of postinfarction ventricular septal defect

Tecklenberg, Paul L.; Fitzgerald, John L.; Allaire, Basil I.; Alderman, Edwin L.; Harrison, Donald C.

doi:10.1016/0002-9149(76)90809-2

Cited by 38 publications

(5 citation statements)

References 12 publications

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“…The value of afterload reduction therapy has been widely documented in both acute [131 and chronic [141 cardiac failure. In addition to its usual beneficial hemodynamic actions in patients with heart failure, nitroprusside may also induce a decrease in the size of the shunt in patients with interventricular septal rupture by reducing afterload and the ratio of systemic vascular resistance to pulmonary vascular resistance [7]; in our patient the shunt decreased from 2.75 to 1 to 1.7 to 1. In the chronic management of our patient, hydralazine maintained the improved hemodynamic performance induced by nitroprusside in the acute phase.…”

Section: Commentmentioning

confidence: 46%

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Chronic oral vasodilator therapy to control heart failure in postinfarction ventricular septal defect

Théroux

et al. 1979

Cathet. Cardiovasc. Diagn.

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This report describes a 70-year-old woman with biventricular failure following an anteroseptal infarction complicated by interventricular septal rupture. Treatment with nitroprusside followed by oral hydralazine eliminated the failure and reduced the shunt from 2.75 to 1 to 1.7 to 1. She is asymptomatic post-discharge. Chronic medical therapy including oral vasodilators may be an acceptable alternative to surgery in a small minority of patients with this complication of myocardial infarction.

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Section: Commentmentioning

confidence: 46%

“…The surgical technique is facilitated and survival is more likely in patients who can be maintained on medical treatment for several weeks postinfarction [4,61. Pharmacologic agents that reduce afterload are useful for this purpose [7].…”

Section: Introductionmentioning

confidence: 99%

Chronic oral vasodilator therapy to control heart failure in postinfarction ventricular septal defect

Théroux

et al. 1979

Cathet. Cardiovasc. Diagn.

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“…The latter, that is isosorbide dinitrate, nitroprusside, and labetalol, lower peripheral vascular resistance and impedance to left ventricular ejection, thereby improving systemic blood flow. 26 27 Synhorst et al28 created ventricular septal defects in dogs. After the administration of vasodilators the size of the shunt was reduced because of the different effects on the total pulmonary and systemic vascular resistances.…”

Section: Discussionmentioning

confidence: 99%

Management of ventricular septal rupture in acute myocardial infarction.

Khan¹,

Patterson²,

O'Kane³

et al. 1980

Heart

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suMMARY Four patients with rupture of the interventricular septum after myocardial infarction are described. This condition carries a grave prognosis. Surgical repair of the septum is almost always urgently required if the left-to-right shunt is large (QP/QS>3). Results are better if surgery can be deferred for six weeks to allow the infarcted area to heal and the tissues to become firmer. This delay may be achieved by using a combination of agents to reduce afterload and to exert a positive inotropic effect. The timing of surgical intervention was an important factor in the survival of three of the four patients.Ventricular septal defect after acute myocardial infarction was first described by Latham in 1846. hours of admission, complete heart block developed, preceded by sinus bradycardia and first and second degree atrioventricular block. The ventricular rate fell to 50/min and the blood pressure to 80/60 mmHg. Temporary atrioventricular sequential pacing was started. The blood pressure rose to 120/80 mmHg. Three days later sinus rhythm returned. The same day severe central chest pain recurred. The electrocardiogram showed sinus tachycardia at 120/min, with further ST segment elevation in leads II, III, and aVF. The blood pressure was 105/80 mmHg. The jugular venous pressure was raised with prominent 'a' and 'v' waves. A loud pansystolic murmur accompanied by a thrill was noted at the lower left sternal edge. A Swan-Ganz balloon tip catheter was inserted at the bedside. A large left-to-right shunt (QP/QS 4-8:1) was confirmed at ventricular level (Table 2). Systolic blood pressure had fallen to 65 mmHg. Digoxin and diuretics were started along with a dobutamine infusion. In view of the size of the shunt, persistent hypotension, and increasing congestive cardiac failure operation was carried out 10 hours after the development of the ventricular septal defect. At operation the right ventricle was greatly enlarged. The inferior surface of the heart was the site of a large haemorrhagic infarct covering most of the base and extending into the mitral annulus. The left ventricle was opened through its inferior surface using a longitudinal incision through the area of infarction parallel to the posterior descending coronary artery. The mitral apparatus and the papillary muscles appeared 570 on 10 May 2018 by guest. Protected by copyright.

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“…In addition, much recent interest has been gener ated in the use of these agents for treatment of acute and chronic pump failure (2 -4 ), potential reduction of myocardial infarct size (5), therapy of severe left sided regurgitant valvular lesions (6,7) or ventricular septal defects (8), adjunc tive therapy for perioperative pump failure (9), emergency treatment of pulmo nary edema (10), and in detection of reversibility and potential viability of dyssynergic wall segments in ischemic heart disease (11). Complications of ni trate therapy may include headache, nausea, flushing, palpitations, postural hypotension, reflex tachycardia, hypoxia (12) and, rarely, methemoglobinemia (13).…”

Section: Introductionmentioning

confidence: 99%

Syndrome of Severe Bradycardia and Hypotension following Sublingual Nitroglycerin Administration

Nemerovski

Shah²

1981

Cardiology

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Severe bradycardia associated with profound systemic arterial hypotension was observed in 3 patients following sublingual nitroglycerin administration. All patients had clinical evidence of active ischemic heart disease. In 1 patient, third-degree heart block was observed several hours later, requiring pacemaker therapy. Radionuclide ventriculography in 1 patient during the bradycardia revealed no significant change in regional wall motion or in left or right ventricular ejection fraction. Review of the literature shows no consistent predictors as to which patients are at risk for developing this syndrome. Possible pathophysiologic mechanisms are discussed. These case reports illustrate an unpredictable and serious complication of nitroglycerin administration, and emphasize the need for caution in use of this drug for ischemic heart disease.

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Afterload reduction in the management of postinfarction ventricular septal defect

Cited by 38 publications

References 12 publications

Chronic oral vasodilator therapy to control heart failure in postinfarction ventricular septal defect

Chronic oral vasodilator therapy to control heart failure in postinfarction ventricular septal defect

Management of ventricular septal rupture in acute myocardial infarction.

Syndrome of Severe Bradycardia and Hypotension following Sublingual Nitroglycerin Administration

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