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Biomedical subjects

G Trevi

Publications and source records attributed to G Trevi.

At least 37 records · Page 2Linked to original sources
PubMed1997

[An intrapatient comparison of adaptation to aerobic and anaerobic exertion during 3 types of physiological cardiac stimulation in chronotropic failure of the sinus node: DDD, VVIR and DDDR].

In sick sinus syndrome with chronotropic incompetence, dual-demand rate responsive pacing (DDDR) may be better than ventricular-inhibited rate responsive pacing (VVIR) and dual-demand pacing without rate responsive function (DDD). In order to compare exercise performance during different activity-driven pacing modes, 15 patients (9 males, 6 females; mean age 59 +/- 13 years), implanted with Synchrony 2020T pacemaker (Siemens-Pacesetter Inc, USA, activity sensor) for sick sinus syndrome, randomly performed 3 treadmill tests (modified Bruce protocol) during DDD, VVIR and DDDR pacing, with pacing heart rate, oxygen consumption (Q-Plex 5000, Quinton), work time, anaerobic threshold and human atrial natriuretic peptide level monitoring. Four patients were excluded from the data results (3 for normalization of chronotropic incompetence, 1 for angina pectoris during rate responsive pacing). Heart rate at the end of exercise was significantly higher during VVIR pacing mode (131 +/- 21 b/min) and DDDR (136 +/- 14 b/min) than during DDD pacing mode (105 +/- 21 b/min), p < 0.05. During DDDR we obtained a significantly higher work tolerance (652 +/- 161 s) and a higher oxygen uptake (22.7 +/- 7.1 ml/kg/min) than during DDD (565 +/- 106 s; 20.1 +/- 6.5 ml/kg/min) and VVIR (599 +/- 155 s; 18.8 +/- 6.5 ml/kg/min), p < 0.05. Also the work time and the oxygen uptake at anaerobic threshold were better during DDDR stimulation (350 +/- 119 s; 14.2 +/- 4.9 ml/kg/min) than during DDD (280 +/- 101 s; 12.2 +/- 4.6 ml/kg/min) and VVIR pacing mode (306 +/- 122 s; 11.6 +/- 4.60 ml/kg/min), p < 0.05. On the contrary, human atrial natriuretic factor values at the maximum exercise were lower during DDD (139 +/- 100 pg/ml) than VVIR (256 +/- 182 pg/ml) and DDDR (209 +/- 195 pg/ml) pacing mode, p < 0.05. In conclusion, DDDR pacing proved to be better than VVIR and DDD in patients with sick sinus disease and chronotropic incompetence.

Adaptation, Physiological↗
PubMed1996

Twenty-four-hour antihypertensive efficacy of felodipine 10 mg extended-release: the Italian inter-university study.

We assessed the 24-h antihypertensive efficacy of an extended-release (ER) 10-mg formulation of the dihydropyridine felodipine in mild-to-moderate essential hypertension [World Health Organization (WHO) stage I-II]. Thirty patients, 23 men and 7 women, aged 37-70 years (mean 53 +/- 9 years) participated in a double-blind, randomized, cross-over study of felodipine 10 mg ER versus placebo. An ambulatory daytime diastolic blood pressure (DBP) >90 mm Hg at the end of a 4-week run-in period was necessary to enter the 10-week treatment phase. Twenty-nine patients completed the treatment phase. Twenty-two underwent a 2-day single-blind placebo follow-up to assess residual drug effects. All patients underwent ambulatory BP monitoring (ABPM) by Spacelabs 90207 recorders. Recorders were programmed to make automatic BP and heart rate (HR) measurements every 15 min throughout the 24 h. Felodipine 10 mg ER significantly (p < 0.01) reduced ambulatory systolic BP (SBP) and DBP values throughout the 24-h, day (7 a.m. to 11 p.m.) and night (11 p.m. to 7 a.m.) periods, but not influencing average ambulatory HR values. Trough-to-peak (T/P) ratios, calculated on the average ambulatory BP values measured in the 7-9 a.m. 2-h interval of the second day of ABPM (before the new drug administration: trough) and in the 10 a.m. to 12 noon 2-h interval of the first day of ABPM (peak BP-lowering effect), were 0.71 and 0.58 for SBP and DBP, respectively. Individual T/P calculations, after post hoc selection of nonresponders, gave superimposable results, the consistency of which was judged on mean, median, and confidence intervals (CI). However, the wide variability of the individual T/P ratios suggests that this method cannot be the only means to evaluate the duration of action of an antihypertensive drug by ABPM. The long-acting BP-lowering drug effect was clearly shown by the ABPM performed in the follow-up when SBP and DBP average values of the 24-h, day, and night periods were still reduced. Felodipine 10 mg ER effectively reduced BP in patients with mild-to-moderate hypertension, showing prolonged duration of its antihypertensive action beyond the time of the next dose.

Adult↗
PubMed1995

Clinical and therapeutic implications of chronic left ventricular dysfunction in coronary artery disease.

In patients with myocardial ischemia, left ventricular dysfunction (LV) may arise from irreversible damage (cell death), myocardial stunning (postischemic dysfunction), or myocardial hibernation (persistent myocardial dysfunction at rest due to underperfusion). Chronic LV dysfunction usually refers to hibernating myocardium. However, stunning might also become chronic, producing persistent myocardial dysfunction. Clinical studies have demonstrated that many patients with coronary artery disease have subsequent recurring ischemic (symptomatic or silent) episodes at short intervals in the same area and that each episode may be followed by myocardial stunning. In these patients the myocardium may not recover fully between episodes and function may remain reversibly depressed for long periods or may even be clinically depressed. The recognition of both stunning and hibernation is very important clinically and therapeutically, since chronic LV dysfunction may have a negative effect on mortality and morbidity in patients with coronary artery disease. Moreover, both clinical states are potentially correctable. Pharmacologic intervention with beta blockers, angiotensin-converting enzyme inhibitors, or calcium antagonists might improve or protect hibernating myocardium. The acute hemodynamic effects of the dihydropyridine calcium antagonist nisoldipine have been investigated in patients with chronic LV dysfunction probably arising from hibernating myocardium. Nisoldipine was found to improve both left ventricular systolic and diastolic function without activating the adrenergic system. The improvement in systolic function may be due to a redistribution of coronary blood flow and to a slight reduction in afterload induced by nisoldipine. On the other hand, nisoldipine may improve diastolic function in these patients by an intrinsic mechanism, Reducing intracellular calcium overload or balancing intracellular calcium homeostasis in the ischemic areas.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic Disease↗
PubMed1995

[Characteristics and clinical course of degenerative aortic stenosis in the elderly].

Degenerative aortic stenosis represents the most common form of aortic stenosis. The aim of this study was to evaluate the relationship between symptoms, valvular disease severity and prognosis. We studied the evolution of valvular aortic stenosis in 65 patients (39 males and 26 females, mean age 77.78 +/- 6.2 years) for a period of 7 years. All patients were submitted to accurate anamnestic examination, ECG, color Doppler echocardiography. Sixteen patients (26%) underwent cardiac catheterization. Associated diseases were: hypertension (45%), diabetes (40%), dyslipidemia (29%), chronic obstructive lung disease (6%). In 64% patients, the diagnosis of aortic stenosis was made after symptoms onset, and in 36% was occasional. Mean age at symptoms onset was 70 +/- 17 years: dispnoea was present in 81%, chest pain in 32%, and syncope in 8%. At the beginning of the follow-up, echocardiography showed, aortic stenosis to be mild in 21.73%, moderate in 60.8% and severe in 17.4%. At the end of the follow-up, mild stenosis was present in 9.5%, moderate in 38.7%, and severe in 51.8%. At entry, 56.6% had pure aortic stenosis, 34.78% had steno-insufficiency and 8.7 had an associated mitral valve insufficiency. At the end of the follow-up pure aortic stenosis was present in 17%, steno-insufficiency in 40%, and associated mitral valve insufficiency in 4.3%. Surgery was performed in 21% of the patients (77% valve replacement and 23% valve replacement and aortocoronary bypass). The mortality, at the end of the follow-up, was 31%. Causes of death were: heart failure (61%), arrhythmias (23%), and surgical complications (16%).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

[Myocardial hypertrophy and arterial hypertension].

Myocardial hypertrophy in different cardiac diseases is considered to be an adaptive mechanism to the increase of hemodynamic load which might restore to normal radius/wall thickness ratio and consequently to normalize wall stress. However, it has been widely demonstrated that beside the hemodynamic load, other factors contribute to the development of myocardial hypertrophy. It has been shown that in hypertensive patients, functional abnormalities (increased contribution of atrial systole to total diastolic filling, increased isovolumic relaxation period, prolonged diastolic duration, slowed ventricular filling and altered diastolic distensibility) precede the development of myocardial hypertrophy. Thus, in hypertensive patients, sign and symptoms of heart failure could be manifested in absence of myocardial hypertrophy, and might be exclusively due to diastolic dysfunction (with normal systolic function). Systolic function might be involved and compromised late when focal myocardial cell death and fibrosis occur and consequently ¿adequate¿ hypertrophy is shifted to ¿inadequate¿. This evolution is accompanied by morphological and functional changes of the myocardium similar to those encountered in dilated cardiomyopathy. Impairment of systolic function in ¿inadequate¿ hypertrophy is also due to structural changes; altered ratio between sarcomers and mitochondria, increased intercapillary distance, sarcoplasmatic reticulum dysfunction, increase of collagene component with a consequent increment of wall rigidity, hypertrophy of arterial tunica media, which alters coronary flow and coronary reserve. The progression of these morpho-functional abnormalities is a very slow process, in which adaptive mechanism mediated by several enzymes and contractile protein, contribute to maintain myocardial viability. However, over the long course, disseminated focal myocardial cell necrosis and fibrosis, which is an evolving process, is considered to be the main responsible factor for the irreversible myocardial damage and systolic dysfunction in advanced myocardial inadequate hypertrophy.

Cardiomegaly↗
PubMed1994

[Elements conditioning the severity of myocardial infarction damage].

The severity of myocardial damage following acute myocardial infarction (AMI) is essentially influenced by the duration of coronary flow interruption during the acute episode. Furthermore the duration and severity of "culprit" lesion before AMI, as well as the presence of adequate collaterals to the culprit vessel represent important factors able to influence the severity of myocardial dysfunction after AMI. Left ventricular damage might evolve progressively depending on the infarct size, the presence of diffuse and severe coronary artery disease and concomitant systemic disease, such as diabetes and systemic hypertension. From a therapeutic point of view, in the presence of irreversible myocardial damage (scar tissue) following AMI medical therapy must be addressed to reduce myocardial consumption and to prevent ventricular dilatation. However myocardial dysfunction following AMI might be reversible (hibernated myocardium). It is of remarkable value the recognition of the hibernated but viable tissue because restoration of normal blood flow, which is the gold standard therapy in these patients, improves myocardial function and clinical outcome in AMI patients. In the presence of hibernated tissue following AMI, pharmacological therapy might temporarily protect the hibernated areas; however, when restoration of normal blood flow (myocardial revascularization) is not performed early, myocardial dysfunction might worsen and progressively evolve becoming irreversible event with restoration of normal coronary flow.

Cardiomegaly↗
PubMed1994

[Mechanisms of transluminal mechanical coronary recanalization].

Coronary angioplasty (PTCA) represents one of the most diffuse technique for myocardial revascularization in coronary artery disease patients. The principal mechanisms, responsible for the luminal increment after successful balloon dilatation are stretching of the vessel wall and splitting of the plaque and its rearrangement in an increased cross section of the vessel. Soon after balloon deflation elastic recoil of the vessel wall might occur at different grades which result in a partial loss of the result achieved by balloon PTCA. This phenomenon seems to be one of the major factors influencing the acute and long-term results of PTCA. Balloon inflation is also followed by endothelial denudation and intramural hemorrhage and intramural thrombus apposition. Then, a proliferative process takes place which is characterised by intimal and smooth muscle proliferation and migration. This process, beside the elastic recoil of the vessel wall, might also contribute to restenosis following balloon PTCA. Other devices for myocardial revascularization were introduced in the clinical practice based on different mechanisms from that of conventional PTCA. Transluminal atherectomy (directional, rotational and rotational-ablation) is based on the removal of plaque material from the vessel, increasing the lumen and creating a smooth surface. By this mechanism of action, plaque splitting and vessel wall stretching might be avoided, thus acute and long-term results are supposed to be improved as compared to balloon angioplasty. Another device for the removal of plaque material is represented by laser angioplasty which utilizes laser energy for the evaporation of the atherosclerotic material and the increase of vessel lumen without vessel wall stretching and plaque splitting.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon, Coronary↗
PubMed1993

[Role of direct coronary angioplasty in the course of acute myocardial infarction].

The application of coronary angioplasty (PTCA) for early mechanical reperfusion in patients with evolving acute myocardial infarction (AMI) was introduced at the beginning of the '80s. There are 5 distinct approaches to PTCA for AMI mainly based on the timing of the intervention: primary or direct PTCA refers to emergency recanalization (as soon as possible) of the "culprit" vessel by the interventional procedure without the use of thrombolytic agents; immediate or sequential PTCA is the combination of administration of intravenous thrombolytic therapy followed very closely by PTCA; rescue PTCA refers to the use of PTCA as a mechanical approach for reperfusion when thrombolytic therapy has failed (60 to 120 min after such therapy has been initiated); deferred or adjunctive PTCA implies coronary angiography and PTCA delayed by at least several days after thrombolytic therapy and reserved for patients with residual ischemia; elective PTCA refers to a delayed symptom-derived procedure after thrombolytic therapy. Immediate PTCA, in which the procedure urgently follows the thrombolytic therapy has been studied in 3 randomized trials (TAMI 1, ECoS, TIMI 2A). All 3 trials have shown that immediate PTCA does not affect positively, but can worsen, the outcome of thrombolytic therapy since it increases mortality and bleeding complication with no improvement in reocclusion rate. Rescue PTCA was evaluated by several Authors who were able to demonstrate that mechanical reperfusion after failed thrombolytic therapy improves prognosis and reduces in-hospital and long-term mortality in this subgroup of patients with AMI. Deferred or adjunctive and elective PTCA represent therapeutic approaches in patients with residual ischemia following a successful thrombolysis able, when residual or recurrent ischemia are present, to prevent major cardiac events and to improve clinical outcome. The major interest was addressed to the role of primary PTCA in evolving AMI, as alternative therapy to thrombolysis. Randomized trials have been able to demonstrate that primary PTCA could dramatically improve the clinical outcome in AMI complicated by cardiogenic shock. Moreover, this approach can be safely performed in patients with contraindications for thrombolytic therapy with excellent results. Despite other advantages, primary or direct PTCA for evolving AMI is still presenting few points which have to be furtherly evaluated: acute or subacute reocclusion rates, restenosis rates, costs and availability to majority of population. The on-going clinical evaluation of other devices for mechanical reperfusion (transluminal extraction catheter-TEC, directional atherectomy, coronary stents, thermal PTCA, prolonged autoperfusion), in order to improve acute and subacute results, could furtherly expand the use of this approach in AMI-patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1993

[Prevention of reinfarction: a global strategy].

Reinfarction occurs in approximately 10-20% of patients with acute myocardial infarction with an year incidence of about 3% for males and 9% for females. The reinfarction induces a worsen prognosis by producing arrhythmias and a new ventricular "remodelling" with an increase in sudden death and cardiogenic shock. The new event may occur, early or later, in regions either adjacent to or remote from the initial myocardial infarction. Among all the patients admitted to our coronary care unit (1181) during the last 6 years, the overall reinfarction rate was 11.4%; among these, 46% were in the same side (SSMI), while 54% in the distant side (DSMI). The SSMI occurred more often during early months after infarction, while the DSMI occurred significantly later. Cigarettes smoking has been shown to be a common and often the only risk factor in patients with early reinfarction; while arterial hypertension, mostly associated with diabetes and hypercholesterolemia, was found the most important risk factor in later reinfarctions. SSMI was strongly related to one coronary vessel disease or to a double vessel disease (especially with interventricular artery and right coronary artery); while DSMI occurred in presence of triple coronary vessel disease involving secondary branches. The later SSMI is related to serious impairment of left ventricular function in 30% of patients, with cardiogenic shock and death evolution in 25%. The clinical trials for prevention of reinfarction showed that the correction of risk factors and the use of anticoagulation and/or antiaggregation therapy, beta-blockers or Ca(++)-antagonist drugs, must be chosen in relation to the myocardial damage related to previous infarct. In all the patients follow-up during the acute, subacute and chronic phases, must be performed by clinical and instrumental controls able to evidence the developing new cardiovascular events in order to decision making.

Decision Trees↗
PubMed1993

[From myocardial hypertrophy to heart failure: role of the interstitium].

In the progression from myocardial hypertrophy to heart failure, abnormalities in the interstitial space of the heart seem to play a critical role. The formation of an extracellular oedema and the alterations in coronary subendocardial perfusion are associated with the development of interstitial fibrosis. Cardiac experimental studies documented the presence of augmented interstitial fluid volume and pressure and a subsequent remodelling of the fibrillar network of the extracellular space of the myocardium during the phases of the cardiovascular response to a sudden overload. Variations of the Starling's forces balance caused by enhanced endothelial permeability or due to an impairment of cardiac lymphatic drainage may contribute to the development of an acute heart failure. During stable hyperfunction, the organization of a chronic oedema should account for interstitial changes in the hypertrophic myocardium. Reactive fibrosis seems to be under hormonal control. The activation of the renin-angiotensin-aldosterone system is responsible for interfascicular and intercellular accumulation of fibrillar collagen within the cardiac interstitium. Perivascular fibrosis in the subendocardium may impair intramyocardial distribution of coronary flow. When an inadequate hypertrophy occurs, because of an elevation in ventricular wall stress, myocardial oxygen consumption rises and this may lead to the exhaustion of coronary blood flow reserve in the subendocardial layers. This underperfusion may be responsible for the development of myocardial ischemia. Coronary hemodynamic changes in the microcirculation as those prompted by interstitial alterations may contribute to the onset of myocyte necrosis and to the formation of restorative fibrosis. The progressive mechanical overload of the spared hypertrophied myocytes could explain the initiation of a positive feedback mechanism which perpetuates endomyocardial perfusion impairment, interstitial oedema and remodelling, finally, causing myocyte deaths and fibrous tissue proliferation. These structural alterations and their pathophysiological counterparts appear to be closely related to the evolution from compensatory hypertrophy to chronic myocardial failure in hypertrophic heart disease.

Acute Disease↗
PubMed1988

Direct visualization of aorto-coronary bypass grafts by two-dimensional echocardiography: a new clinical application.

An attempt was made to assess noninvasively the patency of aorto-coronary bypass grafts by two-dimensional echocardiography (2-D echo) in 21 patients who underwent myocardial revascularization. Fifteen patients had one graft while the other six had two grafts. All 21 patients underwent angiography 6-18 months after operation. A day before angiography a 2-D echo was performed with the aim of visualizing the bypass grafts. In 18 patients with 23 grafts (13 with 1 graft and 5 with 2 grafts) it was possible to visualize the tract of the graft by 2-D echo; 16 were judged patent on 2-D echo and confirmed by selective angiography, while 5 grafts were considered occluded both on 2-D echo and angiography. The other 2 grafts were considered to be occluded on 2-D echo but angiographic control displayed their patency. In 3 patients 2-D echo failed to visualize grafts that were patent angiographically. These data must be considered preliminary and need validation in a larger number of patients. However it is reasonable to conclude that 2-D echo has a reliable capacity to predict graft patency. Such an application may be of value in sequential control of patients with aorto-coronary bypass surgery, especially when combined with other clinical and/or technical data.

Adult↗
PubMed1987

Two-dimensional echocardiography in the diagnosis of intracardiac masses: a prospective study with anatomic validation.

The accuracy of two-dimensional echocardiography in the detection of intracardiac masses was verified in 334 patients who underwent cardiac catheterization in our laboratory over 21 consecutive months. A complete two-dimensional echocardiographic (2DE) examination was performed a day before catheterization. The presence or absence of a mass was verified at surgery in 77 patients who successively underwent mitral or aortic valve replacement (51), left ventricular aneurysmectomy with or without myocardial revascularization (25), and resection of atrial myxoma (2). In 32 patients 2DE revealed the presence of a mass-left or right atrial thrombi in 12, left atrial myxoma in 2, left ventricular thrombi in 16, and endocardial vegetations in 2. The other 45 patients were free of intracardiac masses on 2DE. Anatomic verification at surgery revealed the presence of an intracardiac mass in 34 patients. In 30 (true positives) of these, 2DE revealed the mass as well, and in 4 (false negatives) the presence of a mass had not been identified by 2DE. In 2 patients (false positives) the predicted mass was not found at surgery. Absence of a mass was correctly predicted by 2DE in 41 patients (true negatives). Thus 2DE detected intracardiac masses with sensitivity of 88.2% and a specificity of 95.3%. We recommend that 2DE be performed in all patients prior to hemodynamic study and/or cardiac surgery to enable safer management of patients with intracardiac masses during cardiac catheterization and/or cardiac surgery.

Adult↗
PubMed1985

Plasma levels and urinary excretion of verapamil, norverapamil, N-dealkylverapamil (D617), N-dealkylnorverapamil (D620) following oral administration of a slow-release preparation.

The kinetics of verapamil and of its N-dealkylated metabolites (norverapamil, D617, D620) were studied in six cardiac patients with normal cardiac indexes after 120 mg oral administration of the drug both as conventional preparation and as slow-release preparation. Following a dose of the slow-release preparation, the drug concentration curves were smoother and the mean bioavailability was lower in comparison with the conventional preparation. A patient taking inducing agents (phenobarbital and phenytoin) exhibited a strikingly low bioavailability. Following administration of the conventional preparation, the mean plasma half-lives of verapamil, norverapamil, D617 and D620 were 4.4, 6.6, 8.5, and 15.8 h respectively and the drug concentrations showed a triexponential decay. Urinary excretion data indicate that a saturation phenomenon may occur at level of renal tubular transport and that a competition may be suspected between D620 and the other compounds. It is concluded that various mechanisms, i.e. changes in hepatic and renal clearances, occurrence of a deep compartment, and the properties of the pharmaceutical preparation may affect verapamil kinetics during long-term treatment.

Adult↗
PubMed1984

Diagnostic value of electrocardiogram and vectorcardiogram in postinfarction ventricular asynergy.

The ability of ECG-VCG to predict the severity of postinfarction LV asynergy was evaluated in 152 patients with previous myocardial infarction who underwent left cineventriculography in the right anterior oblique view. Various ECG and VCG signs were examined in order to predict the existence of severe asynergy in general (dyskinesia or akinesia or severe hypokinesia) and of dyskinesia in particular. In patients with inferior myocardial infarction (Group A) persistent ST segment elevation was the only specific ECG sign (100%) of severe asynergy; it had a poor sensitivity (6.2%). Four frontal VCG signs (presence of terminal bite, y- greater than 0.18 mV, maximum early superior vector along x axis = MESV greater than or equal to 1.3 mV, duration of initial superior forces = DISF greater than 50 msec) increased the sensitivity of the ECG-VCG method to 75.8% while maintaining a 100% specificity. Regarding the diagnosis of dyskinesia, only the ECG sign of persistent ST segment elevation and the VCG sign of y- greater than or equal to 0.3 mV had a 100% specificity. The sensitivity of the ECG-VCG method was 33.3% (16.6% ECG and 16.6% VCG). In patients with anterior myocardial infarction (Group B), concerning the diagnosis of severe asynergy, the ECG signs of sigma ST greater than 3 mm in anterior leads; pathologic Q wave in four or more anterior leads (including D1 and aVL); and the presence of LAH or LAH + RBBB, had a 100% specificity and a good sensitivity (60.5%). The VCG sign of a narrow horizontal QRS loop increased the sensitivity of the ECG-VCG method to 71% while maintaining a 100% specificity. As for the diagnosis of dyskinesia, the ECG signs with a 100% specificity were sigma ST greater than or equal to 5 mm in anterior leads, a pathologic Q wave in more than five anterior leads (including I and a VL) and RBBB + LAH; these variables had a sensitivity of 48.3%. The VCG sign of a narrow horizontal QRS loop increased the sensitivity of the ECG-VCG method to 79.3% while maintaining a 100% specificity. In patients with inferior plus anterior myocardial infarction (Group A + B) the signs mentioned above for each group were evaluated, confirming a 100% specificity. Regarding the diagnosis of severe asynergy, the ECG signs had a sensitivity of 61.3%, while VCG increased the sensitivity of the ECG-VCG method to 90.3%.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1983

Cardiac ultrastructure in primary restrictive cardiomyopathy.

A five-year clinical follow-up and the results of myocardial biopsies are described in a patient with primary restrictive cardiomyopathy. Histologic examination of a right ventricular endomyocardial biopsy taken early in the course of the illness was not contributory. Histologic examination of a left ventricular endomyocardial biopsy five years later showed hypertrophy and disarray of myocytes, thickening of the endocardium, and interstitial fibrosis. Connective tissue was compact and regularly oriented in the endocardium, but tangled and irregularly oriented in the interstitium. It is concluded that the irregular network of collagen fibrils and elastic fibers limits diastolic relaxation and prevents ventricular dilatation; that the coexisting hypertrophy results from an attempt to maintain normal pump function; and that the myocyte disarray is a consequence of abnormal mechanical forces generated under conditions of severe fibrosis.

Biopsy↗