Lessons from myocardial contrast echocardiography studies during primary angioplasty.
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Angioplasty, Balloon, Coronary↗
Biomedical subjects
D Czitrom
Publications and source records attributed to D Czitrom.
[Myocardial viability: results of myocardial revascularization during the acute phase of myocardial infarction].
Complete coronary reperfusion after thrombolysis or primary angioplasty is associated with limitation of infarct size and conservation of left ventricular function. The area of viable myocardium recovers its function secondarily, the amount of recovery being related to the precocity of reperfusion. Patients with a patent artery in the acute stage do not all recover segmental contraction to the same extent. There are considerable discrepancies between coronary patency and myocardial perfusion. Myocardial perfusion, measured in the acute phase by myocardial contrast echocardiography is the best predictor of preservation of function. This suggests that microvascular lesions are a sign of the extent and irreversibility of myocardial damage. Modern treatment of infarction should not only restore coronary patency but also ensure effective myocardial reperfusion. The factors which determine recovery of ventricular function after reperfusion during the acute phase, are, in addition to early and complete coronary recanalisation and effective myocardial reperfusion: short duration of ischaemia, small size of the area at risk, collateral circulation, ability of the myocardium to withstand ischaemia, limitation of reperfusion injury. Other factors (smoking, pre-infarction angina, the occluded artery or method of reperfusion) may play a role but the role of confounding factors is always difficult to exclude.
Coronary Angiography↗
Determination of left ventricular cardiac volume by simultaneous radionuclide angiography and measurement of oxygen consumption at rest and during maximal exercise: a comparison of two non-invasive isotopic procedures.
The investigation of left ventricular contractile reserve usually requires the determination of left ventricular volume, but its measurement with radionuclide angiography is difficult. The aim of this study was to determine left ventricular volume directly during exercise by the simultaneous measurement of peak exercise left ventricular ejection fraction (LVEF) and oxygen consumption (VO2max) and to compare the results with another geometric method. In the absence of lung disease, the systemic arteriovenous oxygen difference (DAVmax) during maximal exercise converges to 0.13-0.14 ml O2 per ml blood. The measurement of VO2max allows maximal cardiac output (COmax) to be calculated as VO2max = COmax. DAVmax. By simultaneously determining LVEFex, exercise end-diastolic volume (EDVex) can then be expressed as a linear function of VO2max, maximal heart rate (HRmax), DAVmax and LVEFex. Then, the relationship between end-diastolic counts and true volume can be derived at rest. The two methods were closely correlated (r = 0.91, P < 0.001), despite the geometric method being less accurate when applied to low counting statistic acquisitions. We conclude that rest and exercise left ventricular volume can be determined non-invasively by the simultaneous measurement of VO2max and LVEFex. Furthermore, this method provides additional prognostic information which is clinically relevant in the staging of patients with heart failure.
Adult↗
[Secondary prevention after myocardial infarction; role of beta blockaders].
The betablockers are the most important drugs in the secondary prevention after myocardial infarction. Several studies have shown that, in patients without a contraindication to these drugs, betablockers reduce the mortality and recurrence of infarction by about 25%. The best results observed in the subgroup of patients with criteria of severity (previous myocardial infarction or cardiac failure, left ventricular dysfunction, arrhythmias, residual ischaemia, occluded artery or triple vessel disease) has been shown in the APSI and BHAT studies where the reduction in mortality was almost 50% in the subgroup of patients with cardiac failure. The duration of treatment and the role of betablockers with respect to ACE inhibitors are not as clearcut in 1996.
Adrenergic beta-Antagonists↗
[Indications for heart transplantation (excluding emergencies)].
The improved diagnosis in chronic cardiac failure and the lack of donor hearts have lead to a reexamination of the indications of cardiac transplantation. In the absence of a contraindication, the indication is straightforward in class IV of the NYHA to improve quality of life. In less sympatomatic patients, the primary objectives are to improve the prognosis and prevent sudden death: the indication should be considered with respect to a range of criteria (the VO2 max and arrhythmogenic potential are important features) and the rate of progression of the disease (resistance to treatment, repeated episodes of decompensation). This indication may and should be reevaluated to optimise the distribution of the race donor hearts for the benefit of patient with the most to gain.
Age Factors↗
[Baroreflexes and congestive heart failure].
Abnormal responses are found in the early stages of heart failure with increased sympathetic and decreased parasympathetic activity, causing peripheral arteriolar vasconstriction and tachycardia respectively. The cardiopulmonary baroreflex may be studied by decreasing venous return ("low body negative pressure") and by measuring vascular resistance forearm. The arterial baroreflex may be studied by changing aortic pressures (by intravenous phenylephrine or nitroglycerin). Orthostatism and the tilt test deactivate the cardiopulmonary and arterial baroreflexes simultaneously. These baroreflexes are impaired in patients with heart failure. Their activation does not cause the usual sympatho-inhibition so contributing to increased sympathetic tone. This dysfunction may result from a change at any point on the reflex pathway: the baroreceptors themselves, the afferent, central and efferent pathways. It is selective as during the cold pressor test, the vasoconstrictor response remains intact. One of the possible mechanisms of baroreflex dysfunction in heart failure is loss of sensitivities of the baroreceptors. This may be multifactorial: structural abnormalities, changes in compliance or functional abnormality. Even if the loss of sensitivity is partially related to a change in compliance, other factors play a role. It is more functional than structural abnormalities because, after cardiac transplantation, the baroreceptors regain their sensitivity within 2 to 3 weeks. Excessive Na-K dependent ATPase activation of the smooth muscle cells of the carotid sinus could lead to hyperpolarization of the cell membrane, so reducing the excitability of the receptor. Aldosterone is one of the factors which could activate the Na-K ATPase, as this hormone directly increases pump activity and favorizes the synthesis of new pumps in the vascular smooth muscle cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Autonomic Nervous System↗