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Biomedical subjects

M S Remetz

Publications and source records attributed to M S Remetz.

13 recordsLinked to original sources
PubMed1992

Long-term outcome in patients with congestive heart failure and intact systolic left ventricular performance.

Congestive heart failure (CHF) is typically associated with impaired left ventricular (LV) systolic performance. Few reports exist describing the long-term outcome in patients with CHF and normal LV systolic function. Fifty-two patients initially hospitalized with CHF and intact LV function (ejection fraction greater than or equal to 45%) were followed for 7 years. Mean age when initially identified was 71 +/- 11 years (range 36 to 96), and average LV ejection fraction was 61 +/- 11%. CHF was graded by a clinicoradiographic index, with a mean of 7.0 +/- 2.3 (range 3 to 12, 13 indicates worst CHF). A third heart sound was present in 19 patients (37%), and 17 (33%) had presented with acute pulmonary edema. Principal cardiovascular diagnoses were coronary artery disease in 27 (52%), hypertensive heart disease in 16 (31%) and restrictive cardiomyopathy in 7 (13%). At 7 years, cardiovascular mortality was 46% (24 of 52), and noncardiovascular mortality was 10% (5 of 52). Survival was not correlated with age, principal diagnosis, third heart sound, pulmonary edema at presentation, LV ejection fraction, or presence or degree of LV diastolic dysfunction. Cardiovascular morbidity, consisting of nonfatal recurrent CHF, myocardial infarction, unstable angina or other cardiovascular events occurred in 29% (15 of 52). Combined cardiovascular mortality and morbidity was 75% (39 of 52). In patients with CHF, intact LV systolic function does not confer the same favorable prognosis it defines in other clinical situations. For such patients, the risk of future cardiovascular events is high, a finding that should be considered when designing therapeutic strategies in this group.

Adult↗
PubMed1992

Cardiac evaluation.

Over the past decade there has been a dramatic, rapid development of new imaging modalities used in the evaluation of the cardiac patient. These newer techniques are frequently complex and specialized in their application and interpretation. Nonetheless, the prevalence of cardiac disease in the United States, and the wide application of these diagnostic tests, mandate that the well-rounded clinician has a basic understanding of the utility of these diagnostic modalities. Unfortunately, the burgeoning field of cardiac imaging seems at times to overshadow our most important basic diagnostic tools, namely, the history, physical exam, chest radiograph, and electrocardiogram (ECG). This review will attempt to impart a basic understanding of the newer cardiac diagnostic tests and their utility in various disease states. Emphasis on the importance of the basic clinical exam and the precise integration of specific diagnostic tests into the cardiac evaluation will be emphasized. The article will deliver a basic review of exercise treadmill testing, echocardiography, radionuclide imaging techniques, magnetic resonance imaging, and cardiac catheterization. It is hoped that this review will impart to the noncardiologist clinician a basic understanding of the cardiovascular diagnostic techniques so that an accurate, precise, cost-effective, efficient diagnostic plan for the patient with cardiovascular disease can be developed and applied.

Diagnostic Imaging↗
PubMed1992

Cardiovascular manifestations of connective tissue disorders.

Disease processes that involve abnormalities of the connective tissue are protean in their manifestations because of the ubiquitous and crucial function that connective tissue serves in the body. Connective tissue supports of the heart and vascular structures play an integral role in normal cardiovascular performance, and it is not surprising that many connective tissue disorders produce important pathophysiologic processes that affect cardiac and vascular elements. The article focuses on the cardiac and vascular manifestations of hereditary and acquired forms of connective tissue disease. Special attention is focused on the use of imaging modalities and their role in diagnosing cardiovascular pathology produced by collagen disorders.

Connective Tissue Diseases↗
PubMed1992

Endovascular infections arising from right-sided heart structures.

Endovascular infections that involve the right side of the heart present their own unique etiologies, pathophysiologies, clinical manifestations, and therapeutic issues. The pathology of the vegetations of right-sided endocarditis is identical to that of left-sided endocarditis. These vegetations are irregular, friable masses of varying size the contain platelets, fibrin, RBCs, and microorganisms. These lesions serve as a nidus for deep-seated infection and produce sustained bacteremia. Right-sided endocarditis occurs in 5% to 10% of all cases of endocarditis. The most common predisposing factors are IV drug abuse and congenital heart disease. S. aureus is the most common pathogen. The clinical manifestations include fever, chills, rigor, dyspnea, pleuritic pain, productive cough, and hemoptysis. The cardiac manifestations can be notably absent early in the course of the disease, with only 20% of patients initially showing a significant murmur on physical examination. Peripheral embolic lesions can be seen. Echocardiography is helpful in identifying vegetations on the tricuspid valve in a significant proportion of patients. The chest radiograph is characteristic, showing features typical of multiple septic pulmonary emboli. The radiograph shows multiple, small, fuzzy, patchy, peripherally located densities that can change rapidly on serial films. Complications of right-sided endocarditis include pulmonary infarction, pulmonary abscess, progressive right-sided heart failure, and renal abnormalities. The treatment of right-sided endocarditis includes prolonged therapy, with high doses of IV bactericidal antibiotics. Four weeks of antibiotic therapy is generally required, but newer regimens using combination antibiotic therapy can be successful in sensitive strains of viridans group streptococci and S. aureus. Surgical resection of the tricuspid valve is recommended for organisms that do not respond to initial antibiotic therapy, fungal endocarditis, resistant relapsing organisms, or coexistent infection with S. aureus and P. aeruginosa. The prognosis of right-sided endocarditis is generally favorable when compared with left-sided endocarditis. The prognosis is especially favorable in IV drug abusers infected with S. aureus. Patients infected with fungal organisms, Pseudomonas or Serratia, have a worse prognosis. The presence of significant right-sided heart failure also imparts a worse prognosis.

Anti-Bacterial Agents↗
PubMed1992

The right ventricle in disorders causing pulmonary venous hypertension.

The right ventricle is frequently affected by pulmonary arterial hypertension of postcapillary obstructive origin. The disorders that cause states of pulmonary venous hypertension arise in the left ventricle, left atrium, or pulmonary veins. Biochemical factors, the pericardium, interventricular septum, and pulmonary arterial system combine to communicate the effects of these disorders to the right ventricle. Although not ideally suited to pressure loading, the right ventricle undergoes a series of structural and hemodynamic adaptations that allow for chronic compensation until failure supervenes, with characteristic clinical findings. Exercise may serve to magnify the abnormalities of right ventricular function. Correction of left-sided heart lesions with improvement in pulmonary venous hypertension is associated with favorable effects on the right ventricle. In states of left-sided heart failure, the level of right ventricular function may provide important prognostic information.

Heart Diseases↗
PubMed1991

Validation of continuous radionuclide left ventricular functioning monitoring in detecting silent myocardial ischemia during balloon angioplasty of the left anterior descending coronary artery.

Silent myocardial ischemia has been inferred from transient ST-segment depression during continuous electrocardiographic monitoring. Recently, continuous ambulatory monitoring of left ventricular (LV) function using a radionuclide technique (VEST) has demonstrated episodes of significant silent LV dysfunction in the absence of electrocardiographic changes. To validate the demonstration of silent LV dysfunction with this technique, 12 men were studied during percutaneous transluminal coronary angioplasty. A total of 18 left anterior descending coronary artery balloon inflations were performed. Balloon inflations at 8 +/- 2 atm (4 to 10 atm) lasted 70 +/- 16 seconds. Seventeen of 18 inflations were associated with a decrease in LV ejection fraction greater than 0.10. Mean LV ejection fraction decreased from 0.53 +/- 0.08 to 0.28 +/- 0.11 (p less than 0.0001). In contrast, there was pain in only 10 inflations and ST-segment changes in 7. LV dysfunction was associated with a minimal increase in end-diastolic volume (4 +/- 3%, p less than 0.003), and a major increase in relative end-systolic volume (69 +/- 43%, p less than 0.001). These data suggest that continuous monitoring of LV function with the VEST can sensitively detect silent ischemic decreases in LV function occurring during angioplasty, and provide further validation of the use of this technique for detecting silent myocardial ischemia.

Aged↗
PubMed1989

Predictors of success in percutaneous transluminal coronary angioplasty of chronic total occlusions.

Earlier studies have indicated that percutaneous transluminal coronary angioplasty (PTCA) of chronic total occlusions has a low success rate. To determine success rate and assess clinical and angiographic variables associated with success and complications, 57 total occlusions in 56 patients undergoing PTCA were analyzed. The clinical duration of occlusion was 51 +/- 86 days. Success (less than 50% residual stenosis) was achieved at 40 of 57 (70%) dilatation sites. Of these 57 total occlusions, 5 were attempted within 24 hours of acute myocardial infarction, 35 between 1 day and 8 weeks of clinical occlusion, 13 greater than 8 weeks and 4 were of unknown duration. Success rates were 4 of 5, 25 of 35, 9 of 13 and 2 of 4, respectively, in each group (difference not significant, comparison of all time groups). Of the 9 narrowings with a successful PTCA for an occlusion greater than 8 weeks, the mean duration of occlusion was 93 +/- 41 days (range 60 to 180). None of the attempted dilatations of occlusions with a clinical duration of greater than 180 days (n = 3) was successful. None of the clinical or angiographic variables (including tortuosity, length of occlusion gap, distance of the occlusion from the vessel origin, thrombus, lesion calcium, collaterals, prior myocardial infarction, vessel dilated or diffuse disease) impacted on success rate (difference not significant for all). No patient died, had a Q-wave infarction, required emergency coronary artery bypass grafting or underwent repeat PTCA within 7 days of the procedure. Non-Q-wave infarction occurred in 2 of 56 patients (4%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Mild mitral insufficiency is a marker of impaired left ventricular performance in aortic stenosis.

Whether mitral insufficiency is a marker of decreased left ventricular function in patients undergoing aortic valve replacement for sever aortic stenosis was examined. Hemodynamic measurements in 26 patients with pure aortic stenosis (Group 1), 17 patients with aortic stenosis and grade 1 or 2 mitral insufficiency (Group 2) and 19 control patients were compared. All patients were free of significant coronary artery disease. Ventriculograms were digitized for calculation of ejection fraction, ventricular volumes and wall stress. Despite similar aortic valve areas, Group 2 patients had more advanced symptoms. Cardiac index was comparably decreased in Group 1 (2.6 +/- 0.4 liters/min per m2) and Group 2 (2.7 +/- 0.8 liters/min per m2) compared with the control group (3.8 +/- 0.6 liters/min per m2). Left ventricular end-diastolic and end-systolic volume indexes were increased only in Group 2 (119 +/- 35 and 73 +/- 36 ml/m2, respectively). Likewise, end-systolic wall stress was increased only in Group 2 (149 +/- 54 kdynes/cm2). Ejection fraction was decreased to a greater extent in Group 2 (42 +/- 17%) than in Group 1 (59 +/- 13%) as compared with values in the control group (68 +/- 5%). Although an inverse relation existed between ejection fraction and end-systolic stress in all groups, the ejection fraction (extrapolated to end-systolic stress = 0) was decreased in Group 2, and the slope of the relation was increased in Groups 1 and 2. The end-systolic stress/end-systolic volume index ratio, an index of ventricular performance, was also decreased to a greater extent in Group 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Pulmonary and pleural complications of cardiac disease.

Disorders of the heart frequently cause pulmonary dysfunction because of the close structural and functional association of the heart and lungs. The pulmonary vasculature is very commonly affected by cardiac pathology. The pulmonary vasculature is normally a low-pressure, low-resistance circuit with high compliance and tremendous vascular reserve. Although resting vascular tone is low, there are many identified mediators of pulmonary arterial tone that may help mediate pulmonary blood flow. Alveolar hypoxia is clearly a stimulus for increasing pulmonary vascular resistance although factors that mediate the response to hypoxia are not fully understood. Patients with left-to-right shunting due to congenital heart disease because of elevations in pulmonary artery flow and pressure tend to develop progressive anatomic changes in the pulmonary vasculature. This leads to an increase in pulmonary vascular resistance, irreversible pulmonary hypertension, right heart failure, reversal of shunt flow, and Eisenmenger's syndrome. The degree of anatomic vascular damage due to left-to-right shunting can be graded histologically. Lesser grades of damage are reversible with corrective surgery, whereas more severe grades show no improvement or progression with operation. Chronic left-sided congestive heart failure seen in rheumatic mitral stenosis can cause secondary changes in the pulmonary vasculature. Pulmonary hypertension and increased pulmonary vascular resistance can increase reflexly and form a "second stenosis" that further limits cardiac output. Unlike congenital heart disease, severe grades of pulmonary arterial damage are not seen in left heart failure from mitral stenosis or other causes, and consequently with surgical correction pulmonary hypertension reverses. Pulmonary function testing is adversely affected by congestive heart failure. Both restrictive (stiff lungs) and obstructive (cardiac asthma) defects are observed in congestive heart failure. DLCO is abnormally decreased. With treatment of heart failure these defects reverse. Both elevated systemic and pulmonary venous pressures affect fluid filtration in the pleural space and cause pleural fluid accumulation. The fluid is transudative with low protein, low lactate dehydrogenase, and low cell counts. Transudative effusions from heart failure resolve with treatment. With large effusions and cardiomegaly, pulmonary dysfunction results because of atelectasis from compression and space-occupying effects of the heart and pleural fluid. Following myocardial infarction, cardiac surgery, or other cardiac trauma, the postcardiac injury syndrome can result. The syndrome is characterized by exudative pleural and pericardial effusions along with pulmonary infiltrates, fever, chest pain, leukocytosis, and an elevated ESR. The syndrome must be diagnosed by exclusion of bacterial pneumonia, pulmonary emboli, and congestive heart failure. Treatment is with nonsteroidal anti-inflammatory agents or systemic co

Cardiovascular Agents↗
PubMed1988

Analgesic therapy in acute myocardial infarction.

Parenterally administered narcotic analgesics are a critically important part of therapy for the patient with acute myocardial ischemic syndromes. These agents are very effective and, when used with appropriate caution and monitoring, are also generally safe. They not only relieve the sensation of severe pain but also reduce the effective and physiologic reaction to pain and thus reduce patient anxiety. Because these agents all depress respiratory drive to some degree in the doses used for adequate analgesia, close attention to respiratory status is mandatory. In patients with underlying pulmonary disease or significant congestive heart failure, this monitoring should be even more intensive and include arterial blood gas measurements and preparations for possible narcotic antagonist administration and ventilatory assistance. With regard to the hemodynamic changes produced by these agents, several important points are worth noting. It must be remembered that the conclusions regarding hemodynamic effects of these agents are derived from studies involving patient groups that were generally hemodynamically stable, usually pain-free, and almost always at least several hours following acute presentation. Thus, the hemodynamic effects of these agents may be quite different in patients with active pain during a period of acute ischemia, or in patients that are hemodynamically unstable. Hemodynamic studies during these acute settings, however, are extremely difficult to perform because the patient's acute distress mandates rapid administration of an analgesic agent prior to the institution of invasive monitoring. With these cautions relating to data interpretation in mind, it is still possible to make certain recommendations regarding the use of analgesic therapy in acute MI.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesics↗
PubMed1988

Percutaneous transluminal coronary angioplasty during acute myocardial infarction.

Intravenous thrombolytic therapy with streptokinase in the setting of acute MI has been shown to be effective in improving left ventricular function, limiting infarct size, and improving early mortality. The benefit of this therapy is greatest when administered within 3 hours and is of minimal benefit when given more than 6 hours from symptom onset. Newer second generation thrombolytic agents such as intravenous r-TPA have been shown to be more effective at establishing patency of acutely thrombosed coronary arteries. TPA treatment produces patency rates similar to those observed with intracoronary administration of streptokinase (65 to 75 per cent). This agent will probably become standard therapy for patients with acute MI. Unfortunately, there are significant problems with systemic thrombolytic therapy. The potential for bleeding complications contraindicates the use of this therapy in patients with recent cerebrovascular events, recent surgery, or other possible bleeding problems. Acute angioplasty of the infarct-related artery has been shown to be effective in restoring blood flow in 85 per cent of patients with acute MI. Preliminary studies have suggested that this therapy, when administered within 4 hours from symptom onset, improves global and regional left ventricular function to a greater degree than intracoronary streptokinase. Patients receiving acute PTCA as a primary reperfusion modality have a lower incidence of post-infarction angina and provokable ischemia by exercise testing. If facilities and skilled personnel are available to perform PTCA within 4 hours from symptom onset, this therapy remains an alternative revascularization modality in patients with acute infarction and contraindications to systemic thrombolytic therapy. However, the benefit of PTCA with regard to reduction in mortality when used in this manner is unproven. PTCA can also be used as an adjunctive therapy administered at some time following systemic thrombolytic therapy. Performing PTCA acutely offers the potential to restore blood flow in 90 per cent of the patients that initially fail thrombolytic therapy. However, despite the use of PTCA in this subgroup, benefits with regard to improved ventricular function and decreased mortality have yet to be conclusively demonstrated. Performing acute PTCA following systemic thrombolytic therapy also incurs a high incidence of bleeding complications. If initial thrombolytic therapy reestablishes vessel patency, similar improvements in ventricular function can be expected even if PTCA is deferred until clinically indicated by evidence of recurrent ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)

Angioplasty, Balloon↗