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1/22. Decreased left ventricular filling pressure 8 months after corrective surgery in a 55-year-old man with tetralogy of fallot: adaptation for increased preload.

    A 55-year-old man with tetralogy of fallot underwent corrective surgery. Left ventricular filling pressure increased markedly with increased left ventricular volume one month after surgery, then decreased over the next 7 months, presumably due to increased left ventricular compliance.
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2/22. Case 3: A patient with systemic hypertension and left ventricular hypertrophy.

    hypertension is often referred to as the "silent killer" because most hypertensive patients are asymptomatic until cardiovascular sequelae such as stroke, myocardial infarction, heart failure, or renal failure occur. LVH is a common finding in patients with hypertension, especially African-Americans. Data from the Framingham Heart Study indicate that LVH is an independent risk factor for major cardiovascular events. In the amlodipine Cardiovascular Community Trial, 37% of 124 hypertensive patients screened by means of echocardiography had LVH at baseline. Although there was no difference in the prevalence of LVH by gender or age, African-American patients were nearly twice as likely to have LVH than white patients (64% vs. 34%, p<0.05). Hence, aggressive therapy to reach target goals outlined in the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High blood pressure (JNC VI) is especially important in this group of patients. Even lifestyle modifications such as weight reduction and limitation of salt intake, if sufficiently aggressive, can lead to regression of LVH, as demonstrated by results of the Treatment of Mild hypertension Study (TOMHS). Most classes of antihypertensive drugs are effective in causing regression of LVH. Vasodilators, such as minoxidil and hydralazine, do not have an effect on regression, possibly because reflex tachycardia and stimulation of catecholamines and the renin-angiotensin system associated with these agents may negate the benefit of reduced afterload. There is some controversy regarding the ability of the angiotensin receptor blockers to reduce LVH. In some studies, these agents were associated with regression, whereas in others they were not. Whether targeting LVH as the primary treatment goal in hypertensive patients will have long-term benefits on outcome above and beyond simply reducing blood pressure is not clear.
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3/22. A depressed myocardium.

    BACKGROUND: Venlafaxine is a potent neuronal serotonin and noradrenaline re-uptake inhibitor, and to a lesser extent an inhibitor of dopamine reuptake. paroxetine is a potent selective inhibitor of serotonin reuptake. CASE REPORT: A 27-year-old man ingested 1987.5 mg of venlafaxine and 360 mg of paroxetine. He subsequently developed systolic and diastolic hypertension, transient electrocardiographic abnormalities, and an area of persistent myocardial damage. He recovered from his overdose with his blood pressure and electrocardiogram returning to normal. The area of myocardial damage was documented on echocardiogram as an area of marked hypokinesia at the basal anterior septum. Despite the absence of confirming blood levels or the absolute exclusion of cocaine, this case indicates that venlafaxine and paroxetine have the potential for serious cardiotoxicity when taken in overdose.
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4/22. association of pulmonary atresia with intact ventricular septum and aortic valve stenosis. prenatal diagnosis.

    A rare association of pulmonary atresia with an intact septum was diagnosed through echocardiography in a fetus 32 weeks of gestational age. The diagnosis was later confirmed by echocardiography of the newborn infant and further on autopsy. The aortic valve was bicuspid with a pressure gradient of 81 mmHg, and the right ventricle was hypoplastic, as were the pulmonary trunk and arteries, and the blood flow was totally dependent on the ductus arteriosus.
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5/22. Antihypertensive therapy reduces increased plasma levels of adrenomedullin and brain natriuretic peptide concomitant with regression of left ventricular hypertrophy in a patient with malignant hypertension.

    We investigated the potential role of increased plasma adrenomedullin and brain natriuretic peptide (BNP) levels in a patient with malignant hypertension. A 51-year-old man was admitted to our hospital with a chief complaint of visual disturbance. His blood pressure was 270/160 mmHg on admission. Papillary edema associated with retinal bleeding was observed. echocardiography revealed marked concentric left ventricular hypertrophy with mild systolic dysfunction. plasma levels of adrenomedullin and BNP were markedly elevated. Antihypertensive therapy reduced the plasma levels of adrenomedullin in association with a concomitant decrease in blood pressure. The plasma level of BNP also decreased and regression of left ventricular hypertrophy and normalization of left ventricular systolic function were observed. Our findings suggest that adrenomedullin may be involved in the defense mechanism against further elevations in blood pressure in patients with hypertension and that the plasma level of BNP may reflect left ventricular systolic dysfunction, left ventricular hypertrophy, or both, in patients with severe hypertension.
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6/22. Apical aneurysm and left ventricular hypertrophy.

    A 59-year-old woman presented with an embolic transient ischemic attack and a history of controlled hypertension for 16 years. Both echocardiogram and MRI showed severe biventricular hypertrophy and an apical aneurysm with a thrombus. The occurrence of an apical aneurysm in the presence of cardiac hypertrophy is a rare finding and has been described in patients with hypertrophic cardiomyopathy. However, it has not been reported in patients with systemic arterial hypertension. In this patient the lack of a relationship between the severity of the hypertrophy and the levels of blood pressure, together with the presence of histologic disorganization of myocardial cardiac muscle cells by endomyocardial biopsy suggested the diagnosis of hypertrophic cardiomyopathy.
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7/22. Electrocardiographic changes in patients with cardiac rhabdomyomas associated with tuberous sclerosis.

    BACKGROUND: Cardiac rhabdomyomas associated with tuberous sclerosis induce various abnormalities in the electrocardiogram. Electrocardiographic evidence of ventricular hypertrophy may appear if the tumour is electrically active. To our knowledge, electrocardiographic evidence of ventricular hypertrophy has been reported only in association with congestive heart failure. follow-up studies of changes in electrocardiographic findings are also lacking. methods: We studied 21 consecutive patients with cardiac rhabdomyoma associated with tuberous sclerosis, 10 males and 11 females, aged from the date of birth to 9 years at diagnosis. The mean period of follow-up was 53 months. None of the patients developed congestive heart failure. We evaluated the electrocardiographic changes during the follow-up, and their association with echocardiographic findings. RESULTS: Of the 21 patients, 12 showed one or more abnormalities on the electrocardiogram at presentation, with five demonstrating right or left ventricular hypertrophy. In all of these five cases, the tumours were mainly located in the respective ventricular cavity. In one patient with a giant tumour expanding exteriorly, there was marked left ventricular hypertrophy on the electrocardiogram. Followup studies showed spontaneous regression of the tumours in 12 of 19 patients, with abnormalities still present in only 7 patients. A gradual disappearance of left ventricular hypertrophy as seen on the electrocardiogram was noted in the patient with marked left ventricular hypertrophy at presentation in parallel with regression of the tumour. CONCLUSIONS: The presence of cardiac rhabdomyomas in patients with tuberous sclerosis might explain the ventricular hypertrophy seen on the electrocardiogram through its electrically active tissue without ventricular pressure overload or ventricular enlargement, although pre-excitation might affect the amplitude of the QRS complex. Even in cases with large tumours, nonetheless, the electric potential might- not alter the surface electrocardiogram if the direction of growth of the tumour is towards the ventricular cavity. In many cases, electrocardiographic abnormalities tend to disappear, concomitant with regression of the tumours.
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8/22. Regression of hypertensive nephropathy during three years of optimal blood pressure control.

    Hypertensive nephropathy is among the leading causes of end-stage renal disease. Once renal function is severely impaired, the effects of strict control of blood pressure on the recovery of renal function remain elusive. Published case series suggest that optimal control of blood pressure results in regression of renal failure to some extent. In the present case of biopsy-proven hypertensive nephropathy we show that renal function can substantially improve over time if blood pressure is optimally controlled. Glomerula filtration rate continuously improved in our patient from 20 ml/min at presentation to 80 ml/min over a period of three years using a fivefold antihypertensive regimen. hypertensive retinopathy regressed from stage III to stage I, and left ventricular hypertrophy decreased from an initial septum thickness of 19 mm to 12 mm within that period of time. This case clearly illustrates that optimal control of blood pressure is mandatory in patients with pre-terminal renal failure due to hypertensive nephropathy. Such intervention can lead to a regression of hypertension-associated end-organ injury.
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9/22. Accessory mitral valve tissue causing severe left ventricular outflow tract obstruction in an adult.

    Accessory mitral valve (AMV) is a rare cause of left ventricular outflow tract (LVOT) obstruction and is extremely rare in adults. We report a case of an older adult with an AMV that caused severe LVOT obstruction. A parachute-like piece of tissue (the AMV) protruding into the LVOT during systole was first detected in a 45-year-old woman by echocardiography. Because the pressure gradient and dyspnea gradually progressed, she finally underwent a successful operation for removal when she was 48 years old.
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10/22. Use of the Alfieri edge-to-edge technique to eliminate left ventricular outflow tract obstruction caused by mitral systolic anterior motion.

    A 68-year-old woman with concentric left ventricular hypertrophy, prosthetic valve endocarditis with aortic root abscess, and sepsis had aortic root replacement with an aortic allograft. On weaning from cardiopulmonary bypass, she had hemodynamic instability caused by systolic anterior motion of the mitral valve, which resulted in a left ventricular outflow tract obstruction; the peak pressure gradient across the left ventricular outflow tract was 130 mm Hg, and there was moderately severe (3 ) mitral regurgitation. After reinstitution of cardiopulmonary bypass, a central Alfieri edge-to-edge stitch was placed between the anterior and posterior leaflets of the mitral valve. This reduced the gradient across the left ventricular outflow tract to 10 mm Hg and eliminated the mitral regurgitation, which enabled successful separation from cardiopulmonary bypass.
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