[Biventricular heart pacing and left ventricular heart pacing]. / Stimolazione cardiaca biventricolare e stimolazione cardiaca ventricolare sinistra.

This report describes the case of a 60-year-old patient, affected by alcoholic hypokinetic dilated cardiomyopathy, drug refractory, without surgical indication for ischemic and valvular diseases, implanted with a biventricular pacemaker. The implant was followed by a rapid clinical improvement which allowed the patient's discharge in satisfactory conditions and with strongly reduced diuretic therapy. Ventricular pacing became only left due to increased right ventricular threshold. As a consequence a remarkable decrease in cardiocirculatory compensation was observed, with a new hospitalization due to worsening dyspnea and edema. The instrumental evaluation showed a worsening of the parameters linked to interventricular delay, particularly the interventricular septum activation delay and the reduction in its kinesis. An increase in the ventricular stimulation amplitude led again to a complete capture in both ventricles, with an improvement of interventricular synchronization parameters and septal kinesis. This fact turned into a rapid recovery of satisfactory cardiocirculatory compensation with subsequent patient's discharge.

[Heart rupture in acute myocardial infarct: the advantages of using M-2D color Doppler echocardiography in a coronary intensive therapy unit]. / Rottura di cuore nell'infarto acuto del miocardio: vantaggi dell'uso dell'ecocardiografia M-2D color Doppler in unità di terapia intensiva coronarica.

BACKGROUND: Free-wall rupture of the heart is the second most common cause of death in acute myocardial infarction (AMI), following pump failure. Acute rupture is more common and rapidly fatal, while subacute rupture, which accounts for about 30% of total cases of mortality in AMI, can be diagnosed early by clinical signs with the support of echocardiography in coronary intensive care units. METHODS: From March 1996 to December 1997, 293 patients diagnosed with acute myocardial infarction were admitted to the coronary intensive care unit of our hospital. Of these patients, 71 (23.8%) were treated with thrombolysis within 6 hours of onset of symptoms. All patients were observed daily with M-2D color Doppler echocardiography and in the event of renewed chest pain, electrocardiogram changes, abrupt hypotension, syncope or clinical signs of low output syndrome. RESULTS: We observed 11 cases (3.8%) of free-wall rupture of the heart in acute myocardial infarction with echocardiography, 6 females and 5 males, with a mean age of 74.2 +/- 7.8 years (min. 56-max 84), none of whom had prior AMI. Six of them received thrombolytic therapy, six were hypertensive (54.5%) and three were diabetics (27.2%). Surgical repair was performed in two patients with subacute rupture, but one died a few days later. The echocardiography data at bedside for diagnosis of cardiac rupture were confirmed in 5 patients with autopsy and intraoperatively in two of them. CONCLUSIONS: Routine use of echocardiography in coronary intensive care units allows prompt diagnosis of cardiac rupture in acute myocardial infarction, and in the event of subacute rupture it can accelerate surgical decision-making.

[Threatened paradoxical embolism: its direct visualization by two-dimensional echocardiography]. / Minaccia di embolia paradossa: visualizzazione diretta mediante ecocardiografia bidimensionale.

We describe the case of a 67-year-old patient, who had a stroke with subsequent right hemiparesis two years before coming under our observation. Afterwards he had no more pathological manifestation until he had sudden dyspnoea and marked cyanosis, following a prolonged immobilization due to intervention for slipped disc. Symptomatology regressed rapidly, and few hours later, the patient came under our observation in relatively fair conditions. Echocardiography evidenced moderate enlargement of right heart cavities; by subcostal view we visualized the presence of thrombotic material crossing the foramen ovale. Color Doppler showed moderate tricuspid regurgitation. Pulmonary artery systolic pressure was estimated about 55 mm Hg. The patient was immediately anticoagulated firstly by heparin, and secondly by warfarin, maintaining good clinical conditions. After a treatment of two more weeks he could be discharged with prescription of indefinite anticoagulation. Before discharge an echo examination showed the thrombus was no longer present. Pulmonary systolic pressure was estimated about 40 mm Hg. This is one of the rare cases of direct visualization of impending paradoxical embolus documented in the cardiologic literature.

A brief contact of native whole blood with adenosine diphosphate (ADP) promotes the release of the contents of platelet alpha granules but not dense bodies and increases platelet retention to glass bead columns.

We have previously demonstrated that a brief contact of native whole blood with ADP, promotes a dose dependent release of the contents of platelet alpha granules. In the present study we have shown that in our system there is not a parallel release of the contents of platelet dense bodies as measured by the release of serotonin (5 HT). This early and partial platelet activation determines an increase in platelet retention in glass bead columns. After exactly 15 seconds of activation of native whole blood from 6 healthy volunteers with ADP, in fact, there was a significant fall in the platelet count following the flow of native whole blood across glass beads. A significant decrease (from x = 182,000 +/- 13,700 to x = 120,000 +/- 8,00/microliters p less than 0.001) was present when the blood was stimulated with 0.4 microM ADP final concentration. These results suggest that early, partial platelet activation by ADP could facilitate their possible adhesion to a suitable surface exposed along the vascular tree.

Adenosine diphosphate (ADP)-induced alpha-granules release from platelets of native whole blood is reduced by ticlopidine but not by aspirin or dipyridamole.

A brief contact between native whole blood and ADP promotes a dose-dependent release of platelet alpha-granules without a fall in the platelet number. We assessed the "ex vivo" effect of three widely used antiplatelet drugs, aspirin dipyridamole and ticlopidine, on this system. Aspirin (a single 800 mg dose) and dipyridamole (300 mg/die for four days) had no effect, while ticlopidine (500 mg/die for four days) significantly reduced the alpha-granules release for an ADP stimulation of 0.4 (p less than 0.02), 1.2 (p less than 0.01) and 2 microM (p less than 0.01). No drug, however, completely inhibits this early stage of platelet activation. The platelet release of alpha-granules may be related to platelet shape change of the light transmission aggregometer and may be important "in vivo" by enhancing platelet adhesiveness and by liberating the platelet-derived growth factor.

Repair of ventricular septal defect and aortic regurgitation associated with severe hemophilia B.

A child with severe factor IX deficiency who underwent an open-heart operation using extracorporeal circulation is described. The factor IX level was normalized immediately before operation and at the end of cardiopulmonary bypass by infusing prothrombin complex concentrate and fresh frozen plasma. Partial thromboplastin time and factor IX serum levels were monitored for 20 days postoperatively and showed factor IX activity higher than 50%.

[Thrombolytic therapy with urokinase in 8 patients with massive pulmonary thromboembolism]. / Terapia trombolitica con urochinasi in 8 pazienti affetti da tromboembolia polmonare massiva.

Eight patients with massive pulmonary thromboembolism documented by angiography were treated with Urokinase (UK) 4.400 IU/Kg/hr for 12 hours. UK i.v. infusion was started immediately after angiographic evaluation (Miller index) and was followed by anticoagulant therapy with heparin and sodium warfarin. All patients survived even though 4 pts. were in shock before treatment. Significant reduction of pulmonary obstruction (reduction of Miller index) was obtained in 7 patients with 48 hours from withdrawal of the drug. Mild superficial bleedings which did not influence the clinical course were the only complication recorded. Neither bleedings nor angiographic improvement showed a correlation with thrombin time prolongation. Indications for thrombolytic therapy of pulmonary embolism and particularly prevention of the major haemorrhagic complications are briefly discussed. It is concluded that the high doses of UK suggested by Food and Drug Administration may be used safely in patients affected by massive pulmonary thromboembolism with or without shock, if patients are adequately selected and prevention of major haemorrhagic complications is continued throughout treatment.

Enhanced "in vitro" release of platelet alpha-granules after acute myocardial infarction (AMI).

In vivo platelet activity was studied in 58 patients with AMI on admittance to the Coronary Care Unit, in 48 of these patients after 1 week, in 30 after 1 month and in 24 patients after 6 months. Patients were carefully selected and excluded if they had associated diseases known to increase platelet activity. In vivo activation was studied by evaluating the plasma concentration of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) in the same blood sample. On admittance (x = 58.5) and on day 7 (x = 52.9) beta-TG values were significantly higher than those obtained in the control group (x = 29). beta-TG values were moderately elevated after 1 month (x = 37.7) and then returned to values similar to those of the control group after 6 months (x = 27.9). The simultaneous assessment of PF4 shows a beta-TG/PF4 ratio indicative for in vitro release (less than or equal to 2.5) in many patients on days 1 and 7. Moreover, the beta-TG/PF4 ratio in patients with AMI tends towards 2 when beta-TG values are high. These results may indicate a greater tendency to an in vitro platelet release in the acute phase of AMI.