Diabetic cardiopathy represents a cardiac disorder with involvement of myocardial, interstitial, coronary, and neural structures. One of the main manifestations refers to coronary microangiopathy, which has not yet been clearly identified. Coronary hemodynamics, including the determination of coronary flow reserve, were therefore analyzed in normal subjects and in nine patients with NIDDM and clinically suspected coronary heart disease but normal coronary arteriogram. Coronary flow reserve was determined as the quotient of baseline and minimal coronary resistance after dipyridamole (0.5 mg/kg i.v.). Coronary blood flow was measured quantitatively by the argon method. Systolic left ventricular function was analyzed by ventriculography and diastolic function by M-mode and Doppler echocardiography. Twelve healthy normotensive subjects served as the control group (CON). In the diabetic patients, maximal coronary flow was significantly reduced (172 +/- 50 vs. 395 +/- 103 ml/min x 100 g; P < 0.001), and minimal coronary resistance was increased (0.60 +/- 0.19 vs. 0.24 +/- 0.06 mmHg x min x 100 g/ml; P < 0.001). Coronary reserve in the diabetic subjects was markedly reduced (1.84 +/- 0.39 vs. 4.23 +/- 0.52; P < 0.001). No difference existed with respect to myocardial oxygen consumption (12.4 +/- 2.3 vs. 11.8 +/- 2.8 ml O2/100 g x min; NS). Global systolic function was normal in all patients (ejection fraction: NIDDM 72 +/- 13 vs. CON 77 +/- 12%, NS; CI: NIDDM 3.2 +/- 0.8 vs. CON 3.3 +/- 1.2 l/min x m2, NS). Diastolic function was impaired in diabetic patients with an increase in relaxation time index (97 +/- 23 vs. 45 +/- 18 ms; P < 0.01) and an impaired diastolic inflow pattern, indicated by the ratio between early and late transmitral flow (0.75 +/- 0.14 vs. 1.66 +/- 0.13; P < 0.05). We conclude that the markedly reduced coronary flow reserve in diabetic patients may play a key role in the induction and perpetuation of coronary insufficiency in myocardial ischemia, in diastolic and systolic dysfunction, and in the initiation of diabetic cardiopathy.
The reduced coronary flow reserve in patients with insulin-treated diabetes mellitus may play a crucial role in the pathophysiology of diabetic cardiopathy, causing myocardial ischaemia due to a disturbance of coronary microcirculation leading to diastolic dysfunction and progressing assumably to systolic failure.
Myocarditis is a common cardiological disease. New molecular biological and immunohistological methods have confirmed the persistence of viral infection and chronic myocardial inflammation in a considerable number of patients. A causal link between viral myocarditis and the development of dilated cardiomyopathy has been recognized. This has prognostic implications and helps for the decision of a specific immunosuppressive, immunomodulatory and antiviral therapy.
Mechanical valve thrombosis is a life-threatening event. Pregnancy is associated with a hypercoagulable state that further emphasizes the importance of adequate anticoagulation. This is associated with a therapeutic dilemma. Continued anticoagulation with warfarin throughout the first trimester can result in fetopathic effects, while replacement of warfarin by heparin between 6 and 12 weeks of gestation does not completely prevent the risk of valve thrombosis. There are a small number of reported cases of pregnant women with prosthetic heart valve thrombosis under low molecular weight heparin and consecutive lytic therapy. The authors report a 33-year-old pregnant woman with a St. Jude Medical aortic prosthesis, anticoagulated with a therapeutic dosage of low molecular weight heparin from 6 weeks of gestation, who developed prosthetic heart valve thrombosis at 17 weeks of gestation. A thrombolysis with recombinant tissue-type plasminogen activator (50 mg for 2 hours) was performed. Under thrombolysis, ST-segment elevation in leads II, III, aVF, V5, and V6 developed electrocardiographically with a maximal creatine kinase (CK) of 349 U/L (CK-MB isoenzyme of 48 U/L). Echocardiography revealed normal function of the St. Jude Medical aortic prosthesis 2 hours after thrombolysis and normal wall motions. Short-course thrombolytic therapy appears to be an effective alternative to surgical intervention for the treatment of thrombotic dysfunction of valve prostheses in pregnancy.
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