[Heart rupture during pre-discharge stress test after myocardial infarction]. / Rottura di cuore durante prova da sforzo pre-dimissione dopo infarto miocardico.

A 65-year-old man with a postero-lateral myocardial infarction, complicated by rapid atrial fibrillation was admitted to the Intensive Coronary Care Unit. He received thrombolytic treatment. Electrocardiography and laboratory analysis were suggestive of reperfusion; the rapid atrial fibrillation was converted to sinus rhythm using i.v. amiodarone. Two echocardiograms performed on days 1 and 6 revealed hypokinesis of the postero-lateral wall and a mild reduction in the left ventricular ejection fraction. On day 7, after pharmacological wash-out, he was submitted to a bicycle exercise test: soon after the beginning of the 75 W step, the patient presented cardiac arrest due to electromechanical dissociation and hemopericardium. Despite prolonged cardiopulmonary resuscitation maneuvers and drainage of a few milliliters of pericardial blood, the patient did not survive. At autopsy, a huge clot filling the pericardial space was detected together with two linear 3 cm tears of the left ventricular lateral wall. The authors stress the possibility of unpredictable deaths during a pre-discharge exercise testing; good clinical judgment should therefore be used in deciding which patients should undergo this procedure and appropriate information about its potential risks should be given.

[Acute myocardial damage from a pheochromocytoma]. / Danno miocardico acuto da feocromocitoma.

Cardiac involvement in pheochromocytoma is rare but may be associated with serious clinical deterioration. A 70-year-old woman arrived at our Emergency Department because of chest discomfort, blood pressure lability, mild dyspnea and electrocardiographic signs suggesting an acute myocardial infarction. However two-dimensional echocardiogram did not show any segmental wall motion abnormalities but diffuse and severe left ventricular hypokinesia. The patient was treated with ACE-inhibitors and diuretics and did not receive thrombolytics or beta blocking agents. Creatine kinase-MB and troponin I were normal. Electrocardiogram and echocardiogram completely returned to normal within 1 week and a coronary angiography demonstrated normal coronary arteries. An increase in the catecholamine concentration in a 24-hour urinary sample suggested a pheochromocytoma that was confirmed by abdominal computerized tomography. During surgery, marked hypertension developed treated with sodium nitroprusside and labetalol, and after removal of the tumor severe hypotension required infusion of norepinephrine for several days.

[Progression of cardiopathology in Friedreich ataxia: clinico-instrumental study]. / Evoluzione della cardiopatia nell'atassia di Friedreich: studio clinico-strumentale.

Clinical, electrocardiographic and echocardiographic 5-year follow-up was performed in our institution on 61 patients with Friedreich's ataxia. Cardiac failure was evident in 5% of the patients, and was the most common cause of death. Cardiac arrhythmias, most commonly supraventricular in origin, usually occurred together with the onset of cardiac failure and in 1 case resulted in sudden death. ST-T abnormalities were present in 91% of the cases, and were independent from other clinical parameters. On the contrary, pseudonecrotic (5%) and right ventricular hypertrophy pattern were associated with a poor prognosis. Left ventricular hypertrophy was evident at the echocardiogram in 75% of cases and remained unchanged throughout the entire follow-up period. In 1 case left ventricular hypertrophy turned to dilative cardiomyopathy. Autopsy was performed in 2 out of 4 decreased patients and revealed massive interstitial fibrosis with cellular degeneration in the absence of coronary lesions.

Cardiopulmonary receptor modulation of plasma renin activity in normotensive and hypertensive subjects.

Cardiopulmonary receptors modulate renin release in several animals species. However, their involvement in reflex control of this humoral substance in humans is controversial. Furthermore, no information is available on the alteration of this control in hypertension. We studied the modulation of plasma renin activity (radioimmunoassay) in 12 normotensive subjects and in 12 age-matched subjects with untreated hypertension of mild or moderate degree. Cardiopulmonary receptors were stimulated by increasing central venous pressure (right atrial catheter) and cardiac volume (echocardiographic measurement) through passive leg raising and deactivated by reducing central venous pressure and cardiac volume through lower body negative pressure. The stimuli were maintained for 20 to 30 minutes, and their degree was set to avoid changes in blood pressure (indirect or direct measurements) and heart rate, thus avoiding involvement of arterial baroreceptors. In normotensive subjects, deactivation of cardiopulmonary receptors induced a progressive rise in plasma renin activity and stimulation of cardiopulmonary receptors induced a progressive fall. The reflex gain (ratio between plasma renin activity and central venous pressure or cardiac volume changes) was similar for deactivation and stimulation. During cardiopulmonary receptor deactivation, the gain corresponded to that obtained by dividing the increase in plasma renin by the reduction in central venous pressure induced by tilting. Cardiopulmonary receptor deactivation and stimulation also induced clear-cut changes in plasma renin activity in hypertensive subjects, but the percent magnitude of the reflex plasma renin activity excursion was less than that in normotensive subjects. These observations indicate that cardiopulmonary receptors modulate plasma renin activity in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute and chronic converting enzyme inhibition reduces the vasomotor response to reflex sympathetic activation in man.

Several lines of evidence indicate that angiotensin II (ANG II) may potentiate the vascular response to sympathetic stimulation. However, there are no clear signs that this action of ANG II is physiologically relevant in man. To investigate this problem, we used the lower body negative pressure technique (LBNP, -15 mmHg) to deactivate cardiopulmonary receptors and reflexly stimulate the sympathetic nervous system. The haemodynamic (changes in blood pressure, heart rate, central venous pressure, forearm blood flow) and humoral effects [changes in plasma noradrenaline (PNA) and plasma renin activity (PRA)] of this manoeuvre were examined before and after blockade of angiotensin formation achieved by the administration of the converting enzyme inhibitor, captopril. Studies were performed in patients with essential hypertension in control conditions and after acute and chronic captopril treatment. We found that the reduction in forearm blood flow induced by LBNP was significantly diminished after acute and chronic captopril in spite of the fact that the fall in central venous pressure and the increases in PNA were similar to those observed in control conditions. In contrast, the response of renin to LBNP was enhanced, at least after acute captopril administration. These findings suggest that efficiency of the reflexes originating from the cardiopulmonary receptors is impaired after captopril. Angiotensin II contributes to the vasoconstrictive ability of the sympathetic nervous system, either through a direct vascular action or by enhancing the vascular responsiveness to noradrenaline stimulation. However, this sympathetic facilitatory action of ANG II does not appear to be extended on the adrenergic mechanisms which regulate renin release.

Alterations in plasma noradrenaline in response to reflex modulation of sympathetic vasoconstrictor tone to skeletal muscles.

In man, stimulation and deactivation of carotid baroreceptors are accompanied by sympathetically-induced reduction and increase in total peripheral resistance, but not by alterations in plasma noradrenaline. This has been explained by the inability of arterial baroreflexes to sustainedly modulate sympathetic tone to skeletal muscle vessels on which plasma noradrenaline has been assumed largely to depend. In the present study nine subjects were submitted to procedures that cause a sustained alteration in muscle sympathetic vasoconstrictor tone, i.e. deactivation and stimulation of cardiopulmonary receptors. Cardiopulmonary receptor deactivation was achieved by a 20-min reduction in central venous pressure via application of subatmospheric pressure to the lower body, and the cardiopulmonary receptor stimulation by a 20-min increase in central venous pressure via passive leg raising. Plasma noradrenaline was measured radioenzymatically on blood sampled from an antecubital vein or the right atrium before, and at the 2nd, 5th, 10th and 20th min of each manoeuvre. The noradrenaline measurements were coupled with measurements of arterial blood pressure, heart rate and forearm blood flow and resistance (plethysmographic method). During reduction and increase in central venous pressure, blood pressure and heart rate did not change, whereas forearm vascular resistance markedly rose and fell with a peak response at 5 min and a subsequent plateau. These changes were accompanied by a marked rise and fall in plasma noradrenaline which also peaked within 5 min and were then sustained. Changes in forearm vascular resistance and noradrenaline showed a close qualitative parallelism, each increase in the former being accompanied by an increase in the latter, and vice-versa.(ABSTRACT TRUNCATED AT 250 WORDS)