A 65-year-old man with long-standing hypertension exhibited cardiogenic shock due to the charge of left ventricular outflow obstruction and inexorable mitral regurgitation after surgical repair for abdominal aortic aneurysm.
A 65-year-old man with long-standing hypertension exhibited cardiogenic shock due to the charge of left ventricular outflow obstruction and inexorable mitral regurgitation after surgical repair for abdominal aortic aneurysm. This complication occurr in the early postoperative period and revers immediately after treatment with intravenous verapamil.
somewhat old patients with long-standing hypertension have been fix to have intraventricular gradients localized in the left ventricular (LV) outpouring tract;[1] these patients present with increased LV mass, wall thickness, and shortening fraction.[2] These findings imply a pathophysiologic state in these patients that is highly similar to that found in hypertrophic obstructive cardiomyopathy. The clinical significance and therapeutic recommendations in the vicinity of this condition have not even now been completely defined.
The following is a case of cardiogenic agitation due to the onset of LV efflux obstruction and severe mitral regurgitation in a patient with long-standing hypertension. This complication occurr in the early postoperative period after surgical repair of an abdominal aortic aneurysm and revers immediately after treatment with intravenous verapamil.
CASE REPORT
A 65-year-old man was admitted to the hospital because of suspected hostility of an abdominal aortic aneurysm. The patient had a 20-year history of moderate hypertension. There was no systolic mutter and the echocardiogram showed LV hypertrophy (interventricular septum thickness = 15 mm; LV posterior wall thickness = 13 mm) with normal systolic function. Doppler examination revealed minimal efflux tract gradient (1.5 m/s = 9 mm Hg) and no mitral regurgitation.
Ultrasound and angiographic studies confirmed the diagnosis, and the patient was referr for surgery Surgical repair of the abdominal aorta was performed without intraoperative complications. Four hours after the operation the patient disentangleed severe dyspnea and hypotension (systemic systolic squeezing = 60 mm Hg). Physical examination revealed strait-laced pulmonary edema, shock, and a novel loud holosystolic murmur. Endotracheal intubation and aggressive medical treatment (dopamine, diuretics, plasma expanders) were immediately instituted without any clinical improvement. Progressive hypoxia occurr and cardiogenic onset was documented by a balloon-tipped catheter, which revealed a pulmonary artery urgency of 60/40 mm Hg with a V wave of 50 mm Hg
Echocardiography was therefore solicited Since transthoracic two-dimensional echocardiography was technically inadequate, transesophageal echocardiography (TEE) was performed. This revealed a hyperdynamic left ventricle with reduc diastolic and systolic diameters and without regional wall motion abnormalities. Cavity obliteration occurr in systole and a high LV efflux tract velocity with turbulence was recorded from means of color Doppler imaging. Prominent systolic anterior motion (SAM) of the mitral valve was clearly not absent and associated with severe mitral regurgitation (Fig 1) These data exclud an ischemic etiology of cardiogenic impact and called for a drastic therapeutic decision: conventional therapy for cardiogenic hostile encounter which was ineffective, was discontinued and intravenous verapamil (1 [mu]g/kg/min) was given.
We observ an immediate progressive (30 min) increase in posterity pressure (120/80 mm Hg) and reduction of pulmonary constraining force (40/25 mm Hg). The systolic plaint disappeared, a new TEE consideration (Fig 2) documented the disappearance of SAM and improvement in the strait-laced mitral regurgitation, which became minimal. These changes were associated with a decrease in LV systolic function (from hyperdynamic to normodynamic function) and disappearance of high LV outpouring velocities and turbulence. forward the following day, although hemodynamic and clinical data had steadily improved, an ultrafiltration measure was performed because chest radiography showed the persistence of interstitial pulmonary edema. brace days later the endotracheal tube was remov Clinical, hemodynamic, and chest x-ray data showed the entire resolution of cardiac failure. Ten days later the patient was discharged from the hospital; he was asymptomatic and was maintained forward chronic verapamil therapy.
DISCUSSION
Hypertensive hypertrophic cardiomyopathy is a well-defined condition;[1,2] however, the clinical, prognostic, and therapeutic implications are still being debated, particularly for asymptomatic patients. The not absent case demonstrates that asymptomatic hypertensive hypertrophic cardiomyopathy without significant LV efflux tract gradient or mitral regurgitation may lead acutely to cardiogenic impact and pulmonary edema under certain circumstances.
The TEE research clearly identified the pathophysiologic mechanisms responsible for cardiogenic conflict in our case: hyperdynamic systolic function, LV effusion tract obstruction, SAM, and accurate mitral regurgitation. It has been documented[3,4] in hypertrophic cardiomyopathy that the left ventricle is hyperdynamic and that SAM and defered systolic contact between the mitral valve and the ventricular septum create conformable to fact obstruction to LV outflow; this mechanism increases myocardial wall stres enhances oxygen demand, and abouts mitral regurgitation.
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