Regardless of left ventricle or right ventricle, myocardial ischemia has common clinical characteristics, such as clinical manifestation of chest tightness and chest pain; electrocardiogram manifestation of ST-T changes; management emphasizes myocardial reperfusion and antithrombotic therapy. Compared with left ventricular ischemia, right ventricular ischemia has two major characteristics: rare and concomitant.
The right ventricle is less prone to myocardial ischemia and is associated with less oxygen demand and more oxygen supply.
1, the right ventricular oxygen demand is low: the thickness of the right ventricular wall is 1/3-1/2 of the left ventricle, the weight of ventricular muscle is 1/6 of the left ventricle, the pulmonary vascular resistance is 1/10 of the body circulation, and the work done is only 1/4 of the left ventricle.
2, the right ventricle oxygen supply: the right heart systole on the coronary artery “extrusion” effect is not strong, with systolic and diastolic dual blood supply phenomenon; left crown and right crown between the “pressure gradient”, right myocardial ischemia is also easier to form collateral circulation; right ventricle Thebesian veins are abundant, and the right ventricular myocardium can be directly perfused through Thebesian veins. Right heart ischemia is often accompanied by left heart ischemia. In the region of right coronary innervation, the sharp-edge branch accounts for only a small portion of the right coronary blood flow, and more blood is supplied to the septum, left ventricular lateral wall, inferior wall, and basal segments; therefore, right ventricular free wall ischemia is often accompanied by left ventricular inferior lateral wall and basal segment ischemia; isolated right ventricular myocardial ischemia may occur only when there is a nondominant proximal right coronary stenosis or when the sharp-edge branch is stenosed alone.
Although right ventricular myocardial ischemia is relatively rare and often appears as a concomitant finding of left ventricular myocardial ischemia, the clinical manifestations and management of right ventricular ischemia are somewhat specific, and inadequate recognition or improper management may seriously affect the prognosis of patients. The typical manifestation of right ventricular myocardial ischemia is acute right ventricular myocardial infarction (RVMI), but there are also reports of right ventricular myocardial ischemic angina due to severe non-dominant right coronary stenosis, which are to be discussed separately in this section.
I. Acute right ventricular myocardial infarction
In the early years, the “right ventricular uselessness theory” prevailed in academic circles, which believed that pulmonary artery flow could be generated by elevated venous pressure and right atrial contraction even if the right ventricle was not functional. RVMI is often associated with inferior posterior left ventricular myocardial infarction, and when it occurs, mortality is significantly increased. RVMI alone is very rare (<3%) and is caused by acute occlusion of the non-dominant right coronary.
1. Clinical presentation
About 10% of patients with RVMI may present with significant hypotension, commonly associated with proximal right coronary occlusion and related to the involvement of the acute marginal branch and right atrial branch; it also depends on the left ventricular function. The mechanism of hypotension in the body circulation is a decrease in right ventricular excretion combined with a left septal shift resulting in obstruction of left ventricular filling and a decrease in cardiac excretion. The typical clinical presentation of right ventricular infarction is hypotension, jugular venous filling or angulation, and clear auscultation of both lungs in patients with inferior wall STEMI, known as the RVMI triad. This triad is highly specific (95%) but has a low sensitivity (25%) and is often clinically manifested by hypotension due to lack of jugular venous filling signs due to hypovolemia. Some patients with inferior wall myocardial infarction do not have hypotension at the time of admission, but develop hypotension after the use of nitrates and are diagnosed with RVMI. patients with RVMI may present with Kussmaul’s sign, odd pulses, right ventricular gallop rhythm, systolic tricuspid regurgitation murmur, and arrhythmias (atrial flutter, atrial fibrillation, atrioventricular block).
Therefore, RVMI should be highly suspected when there is unexplained hypotension in inferior wall AMI, a sharp drop in blood pressure after a small amount of nitrates; or Kussmaul’s sign or odd pulse after deep inspiration in inferior wall AMI; or inferior wall AMI combined with atrioventricular block and/or new atrial fibrillation. if timely intervention is not performed, the patient will develop hypoperfusion or even cardiogenic shock, manifested by wet and cold skin The patient will have cold skin, cold extremities, decreased urine output, and altered mental status. The mortality rate of cardiogenic shock due to RVMI is comparable to that of left ventricular, with a mortality rate of 55% to 60% during hospitalization.
2.Laboratory tests
(1) Electrocardiogram: It is an easily available, rapid and non-invasive diagnostic tool. ST-segment elevation ≥1 mm in the right thoracic fourth lead (V4R) has a sensitivity of 70% and a specificity of 100% for the diagnosis of RVMI and is an independent predictor of death during hospitalization. It is noteworthy that V4R is elevated early in the onset and may return to normal 10 to 12 hours after onset. Other ECG changes include ST-segment elevation in leads V1 to V4, ST-segment elevation in lead III > ST-segment elevation in lead II, right bundle branch block and complete AV block.
(2) Echocardiography: It can be done quickly at the bedside and can not only assist in the diagnosis of right ventricular myocardial infarction, but also provide valuable information, such as estimating the function of the right and left ventricles, showing whether there are abnormalities in ventricular wall motion, measuring the size of the right atrial and right ventricular diameters, and estimating the right ventricular systolic pressure; it can also determine whether there are complications of RVMI; more importantly, and in some atypical cases, it can exclude cardiac compression or acute pulmonary embolism.
(3) Coronary angiography: If necessary, coronary angiography can be performed to help clarify the extent of vascular lesions, assess the condition and guide the next treatment.
(4) Serum markers: myocardial markers are an important basis for the diagnosis of myocardial infarction, and troponin is the most specific and sensitive marker of choice for the diagnosis of myocardial necrosis, which begins to rise 2-4 h after the onset of acute myocardial infarction (AMI) and reaches a peak at 10-24 h. Troponin above the upper limit of normal combined with evidence of myocardial ischemia can diagnose AMI. The clinical specificity of myocardial necrosis is high, and its measured value exceeds the upper limit of normal and has dynamic changes during AMI.
3.Differential diagnosis of RVMI
RVMI leads to cardiogenic shock, and its management principles are different from those of cardiogenic shock due to severe left ventricular dysfunction. Therefore, the timely recognition of right ventricular infarction is quite important. Although hypotension, jugular venous filling or anger, and clear auscultation of both lungs are clinically referred to as the RVMI triad, they are also seen in the following conditions: pericardial tamponade, acute pulmonary embolism, severe pulmonary hypertension, right heart outflow tract obstruction, and acute severe tricuspid regurgitation. Constrictive pericarditis and restrictive cardiomyopathy have similar clinical signs, but do not present as acute episodes. Pericardial tamponade, constrictive pericarditis, and restrictive cardiomyopathy can be excluded if the clinical presentation is chest pain with acute inferior wall myocardial infarction and echocardiography suggests right ventricular dilatation and poor function. Acute massive pulmonary embolism can have a similar presentation to severe RVMI, but then the right ventricular systolic pressure does not immediately rise (to 50-55 mmHg or more), and thus severe pulmonary hypertension may be absent. Patients with similar clinical presentation without left ventricular inferior myocardial infarction are suggestive of pulmonary embolism, and the diagnosis can be confirmed by CT or angiography. Acute primary tricuspid regurgitation is often the result of an infected endocarditis bulge and usually has significant echocardiographic changes.
4.Treatment
(1) Reperfusion therapy and antithrombotic therapy: Although right heart insufficiency has the tendency to recover on its own after RVMI, early reperfusion therapy can help to recover right heart function, therefore, direct PCI should be performed as early as possible to rapidly improve the hemodynamic status. If PCI is not available, thrombolytic therapy is feasible. It should be noted that in myocardial infarction caused by proximal occlusion of the right coronary artery, the success rate of thrombolysis is low and the rate of reocclusion after thrombolysis is high because of the hypotension that often accompanies RVMI, so PCI should be preferred in medical centers where it is available, and routine antiplatelet and anticoagulation therapy should be used. Most of the anti-ischemic drugs can cause adverse hemodynamic effects, such as nitrates and vasodilators may induce or aggravate hypotension; β-blockers or calcium channel blockers may cause slow arrhythmias, and these drugs should be used with caution during RVMI.
(2) Maintenance of right ventricular preload: Once RVMI is combined with hypotension or shock, maintenance of right ventricular preload is the main principle of management. Right heart function is significantly dependent on preload, and rehydration can strengthen right ventricular contraction and increase right heart beat volume through Frank-Starling law; moreover, it causes right-left interventricular pressure gradient, and blood flow passively passes through low resistance pulmonary vascular bed. In the absence of signs of left heart failure and pulmonary edema, diuretics and vasodilators such as opioids, nitrates, ACE inhibitors or ARBs should be avoided as much as possible. The principle of “aggressive but not aggressive” should be adhered to for rehydration. The specific method of active rehydration is to infuse NS 200ml for 15 minutes and then 200ml for 30 minutes on the premise of “no left heart failure and no jugular vein anger”. l-2L of fluid is required for most patients in the first 4-6h. Approximately 50% of patients can regain blood pressure with this volume expansion therapy. It is advisable to perform hemodynamic monitoring during volume expansion with CVP <15 mmHg (10-14 mmHg) and PCWP <18 mmHg (15-18 mmHg). When rehydration occurs with elevated CVP without an increase in CO or PCWP >18 mmHg, rehydration is discontinued. It must be noted that RVMI rehydration should not be too aggressive. This is because RVMI is often combined with inferior posterior left ventricular myocardial infarction with underlying left ventricular insufficiency; moreover, a decrease in right heart output with RVMI can mask underlying left heart insufficiency. Therefore, an increase in right heart beat volume by rehydration can stimulate underlying left heart failure. Caution is especially needed when the underlying cardiac function is poor, such as extensive combined left ventricular infarction or a history of myocardial infarction, advanced age, and combined severe valvular disease.
(3) Maintenance of cardiac physiological rhythm: Due to the loss of contractility after right ventricular infarction, maintenance of right cardiac output depends on adequate preload, normal atrial effective sequential pacing and normal ventricular rate. RVMI is prone to sinus bradycardia and AV block due to sinus node and AV node ischemia, myocardial B-J vagal reflex, and medications; RVMI is also prone to atrial arrhythmias due to coronary atrial branch involvement or decreased ventricular compliance, which can lead to atrial ischemia or increased tone; once slow arrhythmias or atrial arrhythmias occur in patients with RVMI, they will induce or exacerbate hypotensive states The patient with RVMI may have a slow arrhythmia or atrial arrhythmia, which will trigger or exacerbate hypotension and require active intervention. In atrial arrhythmias, amiodarone can be used for resuscitation, but attention should be paid to the potential side effects of hypotension aggravated by amiodarone vasodilatation; those with ineffective pharmacological resuscitation or hemodynamic instability should undergo immediate electrical resuscitation. In cases of combined high atrioventricular block that does not respond to atropine, temporary pacing should be provided to increase cardiac output. Right ventricular pacing alone has an important role, but sequential right atrial-right ventricular dual-chamber pacing is more effective. In our experience, isoprenaline should be avoided in patients with acute myocardial ischemia to avoid provoking ventricular arrhythmias.
(4) Positive inotropy: Positive inotropic drugs not only enhance right ventricular myocardial contractility and correct hemodynamic abnormalities, but also have the effect of increasing heart rate and restoring sinus rhythm. If hypotension is still present after treatment with dilation and maintenance of cardiac physiological rhythm, positive inotropic drugs, such as dobutamine, dobutamine, levosimendan and milrinone, are recommended. However, levosimendan and milrinone have certain vasodilating effects and have a potential risk of exacerbating hypotension, so care should be taken when using them clinically.
When drug therapy is not effective, intra-aortic balloon counterpulsation should be considered, which has a significant effect on increasing coronary perfusion pressure and can improve the clinical course and prognosis.
Chronic myocardial ischemia of the right heart
For the reasons mentioned at the beginning, the right ventricle is not susceptible to myocardial ischemia, except in acute, sudden coronary occlusions resulting in acute RVMI. to near normal. Therefore, although the acute phase of RVMI may result in death due to severe hemodynamic disturbances and arrhythmias, the prognosis is generally good after the initial risk period. In clinical studies of chronic occlusive lesions in coronary arteries, good right ventricular systolic function has also been found in chronic RCA occlusions. There is almost no clinical diagnosis of chronic right heart failure due to RVMI alone; nor is there a clinical or pathological diagnosis of so-called “old RVMI”.
However, severe stenosis of the non-occluded right coronary artery can also lead to myocardial ischemia with angina pectoris symptoms. Three cases of non-dominant severe right coronary stenosis leading to exertional angina have been reported to date. 1983 Crosby et al. first reported a patient with post-infarction non-dominant right coronary stenosis leading to stable angina with evidence of myocardial ischemia from decreased right ventricular function during exercise on nuclear imaging. 1996 Zubaid et al. reported a 50-year-old male with typical exertional angina. In 2013 Flynn et al. reported a representative case of a non-dominant right coronary severe stenosis leading to myocardial ischemia and exertional angina. The patient was a 38-year-old smoking male with a family history of hypertension, hyperlipidemia, and coronary artery disease. 2 months prior to the myocardial infarction in the lateral wall, a coronary angiogram showed a dominant gyral branch with mid-segment occlusion, which was treated with stent implantation; the right crown was small (<2 mm in diameter) and innervated only the right ventricle, with 95% mid-segment stenosis. The patient had been complaining of exertional angina (CCS class III) since the myocardial infarction. On review of the angiogram, the gyral branch stent was patent, the anterior descending branch had a mild to moderate stenosis of <50%, and the right coronary lesion was unchanged. In view of the unknown source of chest pain, the patient was examined by FFR: anterior descending branch FFR=0.98, right coronary resting Pd/Pa =0.27, considering right coronary stenosis causing chest pain, no significant residual stenosis after right coronary PTCA balloon dilation, resting Pd/Pa =0.93, FFR=0.79, considering the small vessel, no stent implantation. After surgery, the patient's symptoms were relieved, but three months after PTCA, he had a recurrence of exertional angina, and re-imaging showed 57% resting right coronary restenosis, with resting Pd/Pa = 0.98 and FFR = 0.78. After implantation of a 2.5/15 mm stent, resting Pd/Pa = 0.98 and FFR = 0.85. After PCI, the patient was asymptomatic and could engage in strenuous activity.
This shows that even with a small right ventricular oxygen demand, symptoms can still be induced in severe stenosis of the non-dominant right coronary. This has some implications for clinical interventions: when coronary interventions intervene in the major vessels, attention should be paid to the protection of small vessels in the marginal branches such as the sharp-edge branch, and patients with severe stenosis of small vessels in the marginal branches can still develop angina symptoms.