Medical therapy of aneurysm of the aortic sinus includes blood pressure control through the use of drugs, such as beta blockers.

Another approach is surgical repair. The determination to perform surgery is usually based upon the diameter of the aortic root (with 5 centimeters being a rule of thumb - a normal size is 2-3 centimeters) and the rate of increase in its size (as determined through repeated echocardiography).

Some people live with this type of aneurysm for many years without any specific treatment. Treatment is limited to surgery (ventricular reduction) for this defect of the heart. However, surgery is not required in most cases but, limiting the patient's physical activity levels to lower the risk of making the aneurysm bigger is advised. Also ACE Inhibitors seem to prevent Left Ventricular remodeling and aneurysm formation.

Blood thinning agents may be given to help reduce the likelihood of blood thickening and clots forming, along with the use of drugs to correct the irregular rhythm of the heart (seen on the electrocardiogram)

Medical therapy of aortic aneurysms involves strict blood pressure control. This does not treat the aortic aneurysm per se, but control of hypertension within tight blood pressure parameters may decrease the rate of expansion of the aneurysm.

The medical management of patients with aortic aneurysms, reserved for smaller aneurysms or frail patients, involves cessation of smoking, blood pressure control, use of statins and occasionally beta blockers. Ultrasound studies are obtained on a regular basis (i.e. every six or 12 months) to follow the size of the aneurysm.

Surgery (open or endovascular) is the definite treatment of an aortic aneurysm. Medical therapy is typically reserved for smaller aneurysms or for elderly, frail patients where the risks of surgical repair exceed the risks of non-operative therapy (observation alone).

The size cut off for aortic aneurysm is crucial to its treatment. A thoracic aorta greater than 4.5 cm is generally defined as aneurysmal, while a size greater than 6 cm is the distinction for treatment, which can be either endovascular or surgical, with the former reserved for pathology at the descending aorta.

Indication for surgery may depend upon the size of the aneurysm. Aneurysms in the ascending aorta may require surgery at a smaller size than aneurysms in the descending aorta.

Treatment may be via open or via endovascular means.

Type 1 and Type 2 FAD call for the same treatment: immediate surgery to replace the aorta. Surgery is required due to the high risk of mortality. Type 3 is less severe and requires the maintenance of blood pressure through diet and exercise. Upon diagnosing someone with FAD intravenous antihypertensive treatment is frequently used. Often intravenous sodium nitroprusside is used for its efficiency in lessening the pulsatile load thus reducing blood pressure. Reducing this force slows the progression of the dissection. Surgical success depends on age, severity of symptoms, postoperative organ dysfunction and stroke. Surgical intervention is always indicated in Type 1 cases. Aortic surgery is palliative, not curative. The goal is to merely to prevent rupture, restore blood flow, and fix any aortic valve dysfunction. Post operative protocols include frequent monitoring of the aorta diameter. Statins and beta blockers are also popular treatments used to reduce future plaque build up and blockage of epinephrine receptors as a way to control heart rate and blood pressure.

Long term treatment should also include regular check ups every 3 to 6 months. A CT scan or MRI is recommended, along with required chest x-rays. Antihypertensive therapy with beta adrenergic antagonists is required regardless of medical versus surgical treatment. Ten to twenty percent of those who choose surgical intervention are re-operated on due to compression, aneurysm development or blood leakage.

Aortic ruptures can be repaired surgically via open aortic surgery or using endovascular therapy (EVAR), regardless of cause, just as non-ruptured aortic aneurysms are repaired. An aortic occlusion balloon can be placed to stabilize the patient and prevent further blood loss prior to the induction of anesthesia.

When discovered, hemopericardium is usually treated by pericardiocentesis, a procedure wherein a needle is used to remove the fluid from the pericardial sac. This procedure typically utilizes an 8-cm, 18-gauge needle that is inserted between the xiphoid process and the left costal margin until it enters the pericardial sac, when it can then be used to drain the fluid from the sac. A catheter is often left in the pericardium to continue draining any remaining fluid after the initial procedure. The catheter can be removed when the hemopericardium no longer persists. The underlying causes of the condition, such as over-prescription of anticoagulants, must be addressed as well so that the hemopericardium does not return.

While hemopericardium itself is not fatal, it may lead to cardiac tamponade, which can be deadly if not treated promptly. One study found that cardiac tamponade was fatal in 13.3% of cases in which it was not caused by a malignant disease.

In those with aortic rupture of the AAA, treatment is immediate surgical repair. There appears to be benefits to allowing permissive hypotension and limiting the use of intravenous fluids during transport to the operating room.

No medical therapy has been found to be effective at decreasing the growth rate or rupture rate of asymptomatic AAAs. Blood pressure and lipids should, however, be treated per usual.

Hemopericardium has been reported to result from various afflictions including chest trauma, free wall rupture after a myocardial infarction, bleeding into the pericardial sac following a type A aortic dissection, and as a complication of invasive cardiac procedures. Acute leukemia has also been reported as a cause of the condition. Several cases of hemopericardium have also been reported as a side-effect of anticoagulants. Patients should be made aware of this fact when prescribed these drugs.

Artificial pacemakers have been used in the treatment of sick sinus syndrome.

Bradyarrhythmias are well controlled with pacemakers, while tachyarrhythmias respond well to medical therapy.

However, because both bradyarrhythmias and tachyarrhythmias may be present, drugs to control tachyarrhythmia may exacerbate bradyarrhythmia. Therefore, a pacemaker is implanted before drug therapy is begun for the tachyarrhythmia.

Medical therapy can be initiated with medications that slow electrical conduction through the AV node of the heart such as adenosine (which is a form of pharmacologic cardioversion), beta blockers, or non-dihydropyridine calcium channel blockers (such as verapamil or diltiazem). Numerous other antiarrhythmic drugs may be effective if the more commonly used medications have not worked; these include flecainide or amiodarone. Both adenosine and beta blockers may cause tightening of the airways, and are therefore used with caution in people who are known to have asthma.

Currently, there is controversy over whether or not inheritance truly plays a role in FAD, and if so which gene it acts upon. FAD does not come from strictly one predisposing factor, such as hypertension. It is suggested that the combination of environmental factors along with genetics may contribute to causing FAD. Before newer and more effective cures and therapies can be developed, first the specific gene mutation must be identified. Until such a gene is determined, scientists say patient education, and physician awareness is vital. Currently scientists have found animal models to be beneficial in understanding the pathology behind FAD. In the future there is hope to develop drugs that will better support and strengthen the aortic wall. Endovascular methods of treatment are becoming increasingly popular, and scientists hope to use this technique in both acute and chronic cases.

Historically, the treatment of arterial aneurysms has been limited to either surgical intervention, or watchful waiting in combination with control of blood pressure. In recent years, endovascular or minimally invasive techniques have been developed for many types of aneurysms. Aneurysm Clips are used for surgical procedure i.e. clipping of aneurysms.

Adenosine, an ultra-short-acting AV nodal blocking agent, is indicated if vagal maneuvers are not effective. If unsuccessful or the PSVT recurs diltiazem or verapamil are recommended. Adenosine may be safely used during pregnancy.

SVT that does not involve the AV node may respond to other anti-arrhythmic drugs such as sotalol or amiodarone.

In very rare instances, cardioversion (the electrical restoration of a normal heart rhythm) is needed in the treatment of AVNRT. This would normally only happen if all other treatments have been ineffective, or if the fast heart rate is poorly tolerated (e.g. the development of heart failure symptoms, low blood pressure or coma).

There are currently two treatment options for brain aneurysms: surgical clipping or endovascular coiling. There is currently debate in the medical literature about which treatment is most appropriate given particular situations.

Surgical clipping was introduced by Walter Dandy of the Johns Hopkins Hospital in 1937. It consists of a craniotomy to expose the aneurysm and closing the base or neck of the aneurysm with a clip. The surgical technique has been modified and improved over the years.

Endovascular coiling was introduced by Guido Guglielmi at UCLA in 1991. It consists of passing a catheter into the femoral artery in the groin, through the aorta, into the brain arteries, and finally into the aneurysm itself. Platinum coils initiate a clotting reaction within the aneurysm that, if successful fill the aneurysm dome and prevent its rupture. Flow diverter can be used but not without complications sometimes.

In people without underlying heart disease and who do not have any symptoms, bigeminy in itself does not require any treatment. If it does become symptomatic, beta-blockers can be used to try and suppress ventricular ectopy. Class I and III agents are generally avoided as they can provoke more serious arrhythmias.

If the person is hemodynamically unstable or other treatments have not been effective, synchronized electrical cardioversion may be used. In children this is often done with a dose of 0.5 to 1 J/Kg.

Mortality from aortic rupture is up to 90%. 65–75% of patients die before they arrive at hospital and up to 90% die before they reach the operating room.

IST has been treated both pharmacologically and invasively, with varying degrees of success. IST, in and of itself, is not indicative of higher rates of mortality, and non-treatment is an option chosen by many if they have minimal symptoms.

Some types of medication tried by cardiologists and other physicians include: beta blockers, selective sinus node I channel inhibitors (ivabradine), calcium channel blockers and antiarrhythmic agents. Some SSRI drugs are also occasionally tried and also treatments more commonly used to treat postural orthostatic tachycardia syndrome such as fludrocortisone. This approach is very much "trial-and-error". Patients with IST are often intolerant to beta blockers. A new selective sinus node inhibitor ivabradine is also being used to treat IST.

Invasive treatments include forms of catheter ablation such as sinus node modification (selective ablation of the sinus node), complete sinus node ablation (with associated implantation of a permanent artificial pacemaker) and AV node ablation in very resistant cases (creation of iatrogenic complete heart block, necessitating implantation of a permanent artificial pacemaker).

However invasive treatments can also make the symptoms worse, not cure it. Treatment should be chosen with care as the patient could become in need of a pacemaker or have more extensive symptoms.

Aneurysms can be treated by clipping the base of the aneurysm with a specially-designed clip. Whilst this is typically carried out by craniotomy, a new endoscopic endonasal approach is being trialled. Surgical clipping was introduced by Walter Dandy of the Johns Hopkins Hospital in 1937

After clipping, a catheter angiogram or CTA can be performed to confirm complete clipping.

Emergency treatment for individuals with a ruptured cerebral aneurysm generally includes restoring deteriorating respiration and reducing intracranial pressure. Currently there are two treatment options for securing intracranial aneurysms: surgical clipping or endovascular coiling. If possible, either surgical clipping or endovascular coiling is usually performed within the first 24 hours after bleeding to occlude the ruptured aneurysm and reduce the risk of rebleeding.

While a large meta-analysis found the outcomes and risks of surgical clipping and endovascular coiling to be statistically similar, no consensus has been reached. In particular, the large randomised control trial International Subarachnoid Aneurysm Trial appears to indicate a higher rate of recurrence when intracerebral aneurysms are treated using endovascular coiling. Analysis of data from this trial has indicated a 7% lower eight-year mortality rate with coiling, a high rate of aneurysm recurrence in aneurysms treated with coiling—from 28.6-33.6% within a year, a 6.9 times greater rate of late retreatment for coiled aneurysms, and a rate of rebleeding 8 times higher than surgically-clipped aneurysms.

The mainstay of treatment for CCF is endovascular therapy. This may be transarterial (mostly in the case of direct CCF) or transvenous (most commonly in indirect CCF). Occasionally, more direct approaches, such as direct transorbital puncture of the cavernous sinus or cannulation of the draining superior orbital vein are used when conventional approaches are not possible. Spontaneous resolution of indirect fistulae has been reported but is uncommon. Staged manual compression of the ipsilateral carotid has been reported to assist with spontaneous closure in selected cases.

Direct CCF may be treated by occlusion of the affected cavernous sinus (coils, balloon, liquid agents), or by reconstruction of the damaged internal carotid artery (stent, coils or liquid agents).

Indirect CCF may be treated by occlusion of the affected cavernous sinus with coils, liquid agents or a combination of both.